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Episode 184 - Randy Teel - President & CEO Arvinas · The BioHub - by Avetix

• 0:07
  So welcome back to another episode of the Bio Hub and
• 0:10
  Avetics podcast. Today, I'm joined by Randy
• 0:13
  Thiel, President and CEO of Arvinas.
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  Randy, he has been with Arvinas since 2018, originally joining
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  as Vice President of Corporate Development before progressing
• 0:22
  into more senior leadership roles and ultimately stepping
• 0:24
  into the CEO position. Over that time, he's played a
• 0:28
  key role in shaping the company's strategy,
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  partnerships, and overall growth.
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  Arvinas is one of The Pioneers in targeted protein generation,
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  using its Protac platform to develop therapies that eliminate
• 0:39
  disease causing proteins. In this conversation, we talk
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  about the company's evolutions, the challenges of building a
• 0:46
  platform in biotech, Randy's journey into the CEO role, and
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  what's next for Arvinas. It's a pleasure to have you.
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  How are you? How are you, Randy?
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  Thanks for having us on the podcast, Max.
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  Oh, absolute pleasure. Honestly, I want to start with
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  you and the start of your journey at Avanas.
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  So you've been there since 2018, You've seen the company evolve
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  significantly. What has the the journey been
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  like from your perspective? Well, you're certainly right
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  that the company has evolved pretty dramatically since 2018.
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  So you know, that's eight years ago at this point.
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  And when I joined in early 2018, our Venice had reached a point
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  where it was not yet public. It was still private, not in the
• 1:28
  clinic yet. The company had just nominated
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  its first clinical candidates and it had just completed the
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  Series C financing and was looking ahead to its IPO.
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  So the the company in those days was certainly smaller.
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  I think there were probably 60 or 70 people when I joined.
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  And the major problem at the time, the major issue, I don't,
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  I don't mean problem in a bad way was is this technology going
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  to work right? So the one of the first
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  responsibilities that I had when I joined was preparing for that
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  IPO and talking to a lot of investors and telling the story.
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  And the questions that we were getting asked at that time are
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  very different than the questions we get asked now,
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  right? There were a lot of questions
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  about whether a protect degrader and we'll, we'll get into the
• 2:12
  technology in a moment could ever be delivered orally cross
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  the gut, be a good drug. At the time, our founder, Craig
• 2:20
  Cruz, I think, you know, still very much remembered having
• 2:23
  talked about the technology as a, as a potential parlor trick
• 2:27
  of chemistry. Clearly, we don't get asked that
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  question anymore. You know, I think over the years
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  as we put programs into the clinic, which has now been 6
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  total, we have gone through different phases of clinical
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  trials. We put programs into the clinic
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  in multiple therapeutic areas. We now have had a an initial
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  Phase 3 success with our our ER degrader last year.
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  The transition through all those periods has been pretty
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  dramatic. So the company has grown.
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  The questions have gone from will this technology work to
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  where should it work? Where should we focus?
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  How do you transition from being focused on a platform to how do
• 3:03
  you think about the, the, the programs that we have?
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  You know, the competition set that we have as a company has
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  moved from thinking about ourselves as a Degrador company
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  to thinking ourselves as a therapeutics company where the
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  competition is whatever, you know, whatever program you know
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  is going after the same target or same disease or even broader
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  than that. But I think through it all, you
• 3:24
  know, there have been ups and downs like every biotech company
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  has, but what an incredible ride so far for the first bit of the
• 3:31
  company to have achieved the first that we have.
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  You know, I couldn't be prouder to take on the role of CEO at
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  this point given all that we've achieved.
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  And I and I really think that the best days for our Venice are
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  absolutely coming as we move what is now our our core
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  pipeline of Phase one assets through really important data
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  updates over the next couple of years.
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  And we'll move on to your own progress through the company
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  because I find that's fascinating.
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  But first of all, let let you know Arvinas as a as a company
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  is often seen as one of the leaders in targeted protein
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  degrade degradation. For those less familiar, can you
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  just explain the platform and why it's so exciting?
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  It, it's, it's really simple at its core, which is for decades
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  the pharma and biotech industries have focused on
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  really inhibiting or blocking the activity of proteins, among
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  other ways of working. But that's that's a big one.
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  And the key difference is quite simply that it's a technology
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  that allows us to degrade and completely eliminate a protein
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  instead of just inhibiting its activity.
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  And that's important for a couple of reasons.
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  One is it allows you to better remove the, the, the function of
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  the protein if it's not there at all.
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  Clearly that's better than just inhibiting its function.
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  And just as importantly, a lot of proteins that we as an
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  industry would like to target have multiple functions.
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  So a protein can do more than just one thing, right.
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  So maybe a great example is in our pipeline, the furthest along
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  program is a degrader for LARC 2, which is a target, a kinase
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  target that's relevant in neurodegeneration.
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  And LARC 2 has a kinase function, which is to add a
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  phosphoryl group to a another protein, but it also has other
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  functions. It has a GTP ACE function, it
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  has a scaffolding function, which means that it it, it is
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  involved in a structure where other proteins can build around
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  it and form new functions. And if you only inhibit the
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  kinase activity of LAR two, you might have some effect.
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  But we think that by degrading the protein you affect all three
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  functions, so that the core is that it we're degrading and not
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  just inhibiting proteins. And the way that we do that is
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  by harnessing the natural process that already exists in
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  nearly every cell in the body, right?
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  So cells have a natural way of degrading proteins if they
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  become mutated, if they become dysregulated, if there's simply
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  too much just to maintain a, a normal level of protein.
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  So all the PROTAC degrader does, which is what our technology is,
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  is link disease causing protein of interest like Lark 2 that I
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  just mentioned to that natural cellular machinery which tags
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  the protein and then it gets degraded through the proteosome.
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  And that's the core of it. So it's, it's pretty simple and
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  really combines the benefit of being able to eliminate
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  proteins, which traditionally you might do through genetic
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  therapies or AS OS and things like that.
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  But it allows it to be a therapy that can also be delivered
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  orally because it's, it is a small molecule that we can
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  create as tablets or, or oral formulations, which for patients
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  is often a great option. So it combines really the best
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  of those both worlds. Yeah.
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  And being a platform company you know it comes with it's
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  different set of challenges compared to say a single assets
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  biotech. What what's been some of the
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  biggest challenges you guys have faced?
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  I think the, the core problem or challenge of a platform company
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  is, is capital allocation and how you decide when you are have
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  made enough progress with the platform that you can put
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  programs into the clinic, right. That is.
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  And I think that the word platform, you know, as an aside,
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  I think probably gets overused, but it very much applies here
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  where we have a technology where as I mentioned, you can you can
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  create part of the molecule that binds to the disease causing
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  protein of interest, which of course is different for every
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  program. But you can use a similar other
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  end of the PROTAC, which is what binds to the E3 ligase, which is
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  what I mentioned is that it sells natural machinery.
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  So that has, you know, I think that the dream over time was
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  that you can very quickly, you know, and some investors would
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  have said like Legos, put the different pieces together and
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  very quickly create different programs.
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  I think to some extent that has been true.
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  I think to a greater extent it is, it is still the case that
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  when you create a protector grater, just like every other
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  small molecule, it has to be fully optimized for the use case
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  that you have it for. And I think that the challenge
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  of a platform company is to make progress with the platform, make
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  sure that you can have a repeatable transferable process,
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  get better and better at creating binders to the target
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  proteins, get better and better at creating oral small
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  molecules, things like that. But then also focus on the
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  clinic. And I think some of the
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  challenges that our Venice had, some of the biggest ones and
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  biggest decisions were before I even joined in 2018 where we had
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  had a couple of programs before the ones that ultimately went
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  into the clinic. We had a bet degrader that was
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  in development for quite a while.
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  That was the lead program for the company through 2016 or so,
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  2017, which was really potent and could have been a really
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  powerful drug in preclinical studies.
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  It caused a lot of damage and really wasn't tolerable enough
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  to take him to the clinic, and the company had to very quickly
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  pivot to at some different targets.
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  The first ones that we could took into the clinic were
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  androgen receptor degrader and an estrogen receptor degrader.
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  To do that required some really tough capital decisions.
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  There was a time, you know, well before anybody understood how
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  big I think the protein degrader class could be, the company had
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  to essentially slow all of its research down except for those
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  two programs to get the clinical candidates ready.
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  And then only once we had done that and had shown some initial
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  success were we able to sort of reapply resource back to the
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  research engine and build the pipeline back up again.
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  And that leads that it's a tough question that, you know, when
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  you do it to the decision to slow down research is going to
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  lead to a gap in the future. And of course we had that.
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  We there was that that gap that we went through after AR and ER,
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  but making those decisions is key.
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  You want to make sure the platform stays ahead and is able
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  to produce continued generations of programs which it now has,
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  right, which we now have, you know, are very focused on our
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  phase one programs. But deciding how to progress the
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  platform versus really, you know, button yourselves down and
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  focus on the clinical programs. I think is a problem that you or
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  a challenge that you have less if you're a single or or two
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  asset company where the question is really how can we make this
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  single program get it to the clinic move as fast as possible
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  when you're not trying to trade off maintaining and improving a
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  platform at the same time. See, that's that's really
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  interesting. How do you look at deciding what
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  those targets should be? And also, is that decision
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  affected when you haven't quite made the right choice in the
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  first place? Well, I think that the way that
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  we have long thought about targets was to say a protein
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  degrader is a really important methodology, a really important
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  mechanism, but we never thought it would be the only one, right.
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  So we certainly think that over time, you know, many companies
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  will think about protect degraders the same way they
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  think about antibodies and other therapies.
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  Nobody asks the question, you know, sort of no one asks an
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  antibody company what makes you the best antibody company.
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  There will always be, I think a great use case for many of these
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  modalities that we have. Our goal has been to find the
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  place where it makes sense to have a protectorator.
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  So it's not just where we think we can get a little bit
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  different of a, of a of an efficacy effect.
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  It's to go places that inhibitors have not been able to
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  go or we think that the mechanism that I described would
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  make a big difference. So a couple examples.
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  First, going back to LAR 2 that I mentioned before, there are
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  inhibitors of LAR 2 not in the market but on the clinic and we
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  think that by degrading and not inhibiting the kinase function,
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  we will eliminate the whole protein and really impact kinase
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  function. We also think that the neuro
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  inflammatory effects that are caused or could be helped by
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  degrading the protein itself for LAR 2 will be an additional
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  advantage over LAR 2 inhibitor. To go another direction, we have
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  a degrader called ARV 393 for a target BCL 6, which is relevant
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  in hematology. There had been a number of of
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  efforts to create an inhibitor for BCL six that really didn't
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  get the into the clinic or very far if they did get there.
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  And we think that a degrader is a much better approach.
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  One reason for that is that BCL 6 is an incredibly rapidly
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  resynthesized protein. If you inhibit it or you knock
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  it down, it comes back to its normal steady state level really
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  quickly. So it's important to get really
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  deep levels of levels of degradation and inhibiting.
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  It doesn't seem to have provided that effect.
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  Now we have now have ABCL 6 degraded that's in the clinic
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  hasn't shown data yet, but we have been fortunate to say last
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  fall that even at doses that we didn't predict to be to produce
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  efficacious exposures, we've already seen some responses.
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  We've got a competitor with the BCL 6 degrader who's also shown
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  some great initial Phase 1 results.
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  And, and I think it's, it's looking for those opportunities
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  where a degrader isn't just a little better, but is doing
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  something that an inhibitor can't do is a key.
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  The other one is, is rooted administration too.
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  I'll go back to neuroscience. A lot of our competition that we
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  will face in drugs for neurodegeneration will be
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  against things like anisense oligonucleotides or antibodies.
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  Well, antibodies get into the brain, but only just barely.
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  They really have to dose pretty high to get any effective dose
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  in the brain and clearly is not going to be an oral therapy if
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  it's an antibody. Similarly an anesense
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  oligonucleotide can get into the brain, but again less so than a
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  small molecule can has to be delivered intrathecally.
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  And we don't think actually can often penetrate deep into the
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  brain regions where you're going to need to go in order to have a
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  therapeutic effect, therapeutic effect.
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  And we've shown that with a small molecule protect degrader,
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  we can, we can dose orally, we can cross the blood brain
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  barrier, we can degrade in deep brain regions.
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  This is, I'm talking right now about non human primate data,
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  but that's a clear advantage for a patient versus an IV or an
• 14:10
  intrathecal therapy. Yeah, it's awesome.
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  I think what you guys are doing is really interested in like
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  there's a reason you, you're a name in the industry.
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  I'm also like, I, I love your own progression within the
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  company. You know, we talked about how
• 14:28
  you started AVP corporate development and chief business
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  officer and, and now CEO. How's that transition been and
• 14:36
  what's been the the biggest learning curve?
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  Yeah, well, the, I mean, the, the biggest learning curve, we
• 14:42
  can talk about the transition too, but the, I would say the
• 14:44
  biggest learning curve. I got asked this exact same
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  question in a town hall not long after I was named CEO.
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  And they said, what's the biggest surprise?
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  And I don't think I answered it very elegantly, but the the
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  answer is really something that we all know, which is that
• 14:59
  everything is more complicated than you think it is, right.
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  And I'll get to what you do about that in a moment.
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  But I think that's true of everybody in a company, no
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  matter what part of the company you grow up in, right.
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  So my background, I started off as a scientist in immunology,
• 15:14
  but over the years very clearly progressed to the business side
• 15:17
  of, of, of biotech. But I know from my days in
• 15:20
  science that everything in the lab is far more complicated and
• 15:23
  far more difficult and far more challenging than it appears to
• 15:26
  me when it gets to my, my proverbial desk.
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  As Ceoi know from my time in, in the, the GNA functions like
• 15:33
  strategy and business development that even in those
• 15:35
  areas where the ultimate deliverable is a recommendation
• 15:39
  or a decision or a PowerPoint deck articulating that, the
• 15:42
  thinking that goes into it is far more detailed and intricate
• 15:45
  and complicated than it is by the time it gets to gets in
• 15:49
  front of the CEO. And so as I've taken on this
• 15:52
  chair, right, I've seen the same thing over and over again and
• 15:55
  all the other functions that I've spent less time in.
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  And I think it's always, it always behooves us leaders to
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  remember that just as I know how complicated things are and how
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  difficult they are in every function that I've been part of,
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  that's true everywhere. And So what do you do about
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  that? I think is very clearly the job
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  I have now is to provide some structure, right?
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  The job I have now is to understand decisions and create
• 16:20
  the the the conditions for the great leaders that we have to
• 16:24
  make well thought out decisions and making that work well, at
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  least internally, I see as my as as my most important job, right.
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  And making sure that the teams understand each other, making
• 16:35
  sure that I understand not just what the recommendation is, but
• 16:39
  what recommendation it isn't. What were the key areas of
• 16:42
  disagreement? Like if this recommendation
• 16:44
  turns out in two years to have been wrong, like let's all put
• 16:47
  money on why we think that might have been.
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  What's the weakest part of the thinking, And I think that has
• 16:52
  been the biggest learning is that in, again, it shouldn't be
• 16:54
  a learning at all because I know it from the areas that I grew up
• 16:57
  in. But but everything that you
• 16:59
  start to put to look, look into is more complicated and and
• 17:02
  providing that structure is what we as leaders need to do most
• 17:04
  importantly. Yeah, it's a different aspect,
• 17:08
  right? Like everyone's looking at you
• 17:09
  for for those decisions as well. It's just a step up in in
• 17:13
  everything that you know how to do, but just to added pressure.
• 17:16
  Yeah. One of the more unique aspects
• 17:20
  for you guys recently is the decision to go with Pfizer to
• 17:24
  look for another partner. I I just want to hear more about
• 17:28
  that. I find it really interesting.
• 17:30
  I think, I think you said it's unique, that is to our knowledge
• 17:34
  correct. So we are definitely doing
• 17:36
  something here that I I don't think has a lot of precedent, at
• 17:39
  least we haven't heard that it does.
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  And the the back story here is, is the most important piece I
• 17:44
  think right, which is our lead program is partnered with
• 17:47
  Pfizer. It's an estrogen receptor
• 17:49
  degrader for breast cancer called that Degastrep.
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  And we did a deal with Pfizer back in 2021 on that program,
• 17:56
  which is a 5050 Co development Co commercialization, which
• 17:59
  which was phenomenal for the program and for the company.
• 18:02
  It was a a billion dollar, you know, split across an upfront
• 18:06
  and across an investment from Pfizer that really changed the
• 18:09
  face of the company for sure. And for that program we ran a
• 18:13
  pivotal trial called Veritech 2 that read out its top line data
• 18:16
  last March, in March of 2025. And to some extent it showed
• 18:21
  exactly what everyone would have predicted, which is in late line
• 18:25
  breast cancer where many of the patients have have tumors that
• 18:30
  are driven by estrogen receptor, but many of them don't.
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  Many of those tumors are not driven by estrogen receptor.
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  The there's a mutation in ESR one.
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  And if a patient has that ESR one mutation, they are typically
• 18:43
  thought to respond to an ER therapy.
• 18:45
  Well, Bebdeca strength in ER therapy.
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  And lo and behold, we had a positive pivotal, you know,
• 18:49
  readout in that population. We didn't have a positive
• 18:53
  readout in the all comers population, which includes a lot
• 18:56
  of the patients who are not believed to be driven by ER.
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  That didn't surprise us very much.
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  And and this is the third ER therapy, first Protac, but the
• 19:05
  third ER therapy in this similar setting and the first who had
• 19:09
  seen the same thing. So on one hand it wasn't, it
• 19:11
  wasn't much of a surprise in in the wake of those data, Pfizer
• 19:16
  decided that they didn't want to go forward with the development
• 19:19
  program that we had together, which was further combination
• 19:22
  trials in the first line and in the second line breast cancer as
• 19:25
  well. And with that decision that
• 19:28
  Degustrint really became a second line monotherapy drug.
• 19:32
  We still believe it could be best in class.
• 19:34
  We are awaiting a decision from the FDA on that program.
• 19:36
  It's not approved yet, but we have every reason to believe it.
• 19:39
  It will be a best in class program and we look really
• 19:42
  forward to getting that program to physicians and to patients.
• 19:45
  But we had a decision to make as a company that if it was going
• 19:49
  to be a decision of are we going to build a commercial team and
• 19:53
  infrastructure to launch a therapy or are we going to take
• 19:58
  the capital that we could have done use that for and apply it
• 20:01
  to a really exciting early stage pipeline and still have that
• 20:05
  Degustrint get to patients just in the hands of another company.
• 20:08
  But we chose the latter, right. We said that that will still get
• 20:12
  to patients. We're looking with Pfizer.
• 20:15
  Pfizer has been a good partner, has to find a new partner to
• 20:17
  commercialize the the drug. And we've chosen to focus our
• 20:21
  resources on what is now 4 phase one assets across neurology,
• 20:26
  hematology. I haven't mentioned the ones in
• 20:29
  solid tumor oncology which is AK Rescue 12D program and we just
• 20:33
  put another program in the clinic for a rare disease called
• 20:36
  Kennedys in the past few months. That's the decision we made.
• 20:39
  We we think that we can create more value for patients and for
• 20:42
  shareholders by taking the next generation of protect degraders
• 20:45
  that we have and letting someone else launch them.
• 20:48
  I'll also add there that early in the conversation I mentioned
• 20:52
  an AR degrader. We out licensed our AR degrader
• 20:55
  called Luxdigalutamide to Novartis a couple of years ago.
• 20:58
  That program continues to move along really well.
• 21:01
  They've got it in three different accommodation studies
• 21:03
  from early stage to late stage prostate cancer.
• 21:05
  And I think it's, it's AI said, I felt fortunate.
• 21:08
  I feel fortunate because our Venice now has four programs in
• 21:12
  phase one that all have data coming up in the next year or
• 21:14
  so, some of which are just it's very soon.
• 21:18
  And we have all that with the foundation of Vepdeg, which has
• 21:21
  positive pivotal 3 phase three data, the foundation of Luxdeg,
• 21:25
  which is now with Novartisan moving forward and we've got the
• 21:28
  capital to move to our inflection points.
• 21:29
  So as the first time CEO, I'm pretty excited about that, that
• 21:33
  range of options, but that might have been more background than
• 21:35
  you needed. But that's that really explains
• 21:37
  the decision with Pfizer on VEP and I think explains why we're
• 21:41
  going the direction we are as a company now.
• 21:44
  That's perfect. I mean, for me though, it's
• 21:47
  like, how do you then balance that pipeline alongside, you
• 21:51
  know, balancing the, the platform development and all of
• 21:55
  that? There's a lot, there's a lot of
• 21:56
  moving parts, right? That's definitely true.
• 21:59
  And I think that as we've as we've talked about the
• 22:01
  transition we've made, you know, we've we've now gone from a
• 22:04
  company where the focus a year ago was very clearly working
• 22:08
  with Pfizer to get Vepdeg launched and to patients and to
• 22:12
  use the, you know, the revenues that would come from that to put
• 22:15
  back into the pipeline that we have.
• 22:17
  We've now decided to move forward solely with that
• 22:19
  pipeline again with the foundation that I mentioned.
• 22:21
  And I think you know going back to the the question you asked
• 22:25
  before about platforms and pipelines, right, the key shift
• 22:28
  that we've made here is very clearly to the pipeline.
• 22:31
  That is not at all to say that the platform is not important,
• 22:34
  but we know that to move forward a the rich clinical pipeline
• 22:37
  that we have that's going to take some money.
• 22:40
  You know right now it is a case where each of those programs is
• 22:44
  in phase one. Phase 1's have this habit of
• 22:48
  turning into phase Two's, right? Monotherapy trials have a habit
• 22:51
  of turning into combination trials, especially in oncology
• 22:54
  for drugs like 393, which is the BCL 6 degrader or ARV eight O 6,
• 22:58
  which is the KRAS G12D degrader that I mentioned.
• 23:01
  So we know that going ahead we're going to have to continue
• 23:04
  making choices about where our Venice plays to win.
• 23:07
  We have a very strong history of partnering even before the
• 23:10
  program deals that I mentioned with Pfizer and with Novartis.
• 23:14
  We had a long history of doing platform target based deals all
• 23:18
  the way back to I want to say 2013 when the company was found.
• 23:22
  It might have been 2014, but very early when the company was
• 23:24
  founded. And so it's important to make
• 23:27
  sure that we can progress the pipeline first and foremost
• 23:30
  while making sure that the platform which has been
• 23:33
  amazingly productive and the programs that we put into the
• 23:36
  clinic have done what they said they were going to do right.
• 23:39
  They have the the preclinical results have really translated.
• 23:42
  I think we, we probably are guilty of not, not not being as
• 23:47
  proud of as as we should be of how many firsts that we've made,
• 23:52
  how unusual it is that a new therapeutic modality comes to
• 23:56
  the table and moves as quickly as degradation has.
• 23:58
  Like I said, we put six programs in the clinic now there's lots
• 24:01
  of other companies in the space and we're rooting for all of
• 24:04
  them for this new modality, which we think, you know, very
• 24:07
  much could be at the table with traditional small molecules and
• 24:10
  antibodies. Genetic therapies, as you know,
• 24:13
  a part of the core group of therapies that industry
• 24:16
  considers as they figure out what the right technology is for
• 24:19
  each target we want to hit. Yeah.
• 24:22
  Yeah, I love what you guys are doing.
• 24:23
  Like, you know, you've been around for a fair while, but
• 24:26
  like really achieving some some awesome things.
• 24:29
  I just want to give you the spotlight as well.
• 24:32
  We spoke about that this a little bit when we first met
• 24:36
  you. You're a really strong advocate
• 24:38
  for the biotech ecosystem in Connecticut.
• 24:41
  What what makes that region so interesting?
• 24:44
  And you know, also, how do you see it evolving?
• 24:45
  So I I'm not originally from Connecticut.
• 24:48
  I came here for grad school 25 years ago this year.
• 24:51
  And when I got here again for a program in immunology, I think
• 24:56
  as people thought about biotech or pharma in Connecticut, they
• 24:59
  thought about Bayer and the talk, thought about BMS and
• 25:03
  Wallingford and Pfizer up in Groton and Beringer, Ingelheim,
• 25:06
  the big ones, right? It's not that there weren't any
• 25:08
  small companies here. Alexion, which I, which I later
• 25:10
  joined was certainly here in 2001 in a very different format
• 25:14
  that it's in now 454 Life sciences.
• 25:17
  There's, there's been a number of them over the years.
• 25:20
  And I think that we have reached a point where we've got, we've,
• 25:23
  we've always got a couple of fairly stable larger companies.
• 25:27
  And I include our Venice in that.
• 25:29
  Our Venice is here, Biohaven is here.
• 25:31
  But we've also had some really great examples of companies that
• 25:35
  have been successful and turned over and had people say, look, I
• 25:39
  want to be here in Connecticut. I don't want to go to Boston or
• 25:42
  San Francisco. And so they've moved on from
• 25:45
  from Locks Oncology, which was in Stanford.
• 25:48
  They've moved on from from from a Halda, which is sold to J&J
• 25:53
  earlier this year and are now sort of recycling through the
• 25:55
  biotech industry in New Haven, but also in in Connecticut more
• 25:58
  broadly. And look, sometimes when I get
• 26:01
  asked this question, people want to compare it to Boston or San
• 26:03
  Francisco. I think that's a bad comparison.
• 26:05
  I don't think that's the right. I don't think that's the right
• 26:07
  aspiration. I think there are always going
• 26:10
  to be secondary biotech regions, right?
• 26:13
  And I think New Haven and Connecticut fit right into that
• 26:16
  where you've got a critical mass of great people.
• 26:18
  You know, as I talked about the transition from the focus on
• 26:21
  some of those other companies back in 2001, BMS is gone,
• 26:25
  right? BMSA lot of folks from BMS
• 26:27
  stayed in Connecticut and are now at places like our Venice
• 26:30
  and Bio Haven and others. We've done a great job as a
• 26:33
  local industry picking up the best talent and and keeping them
• 26:37
  here in Connecticut. And I hope we continue to do
• 26:39
  that and our Venice is certainly committed to doing that.
• 26:43
  Definitely, definitely amazing that I know.
• 26:46
  That brings us to to the final question, which is a question I
• 26:48
  ask everyone. If you could have dinner with
• 26:51
  any scientist or innovate, past or present, who would it be and
• 26:55
  why? My answer to this question has
• 26:57
  probably changed since taking the CEO role on.
• 26:59
  You know, I've, I've mentioned that I started off with a APHD
• 27:02
  in immunology and then quickly jumped over to the business
• 27:05
  side. I was a management consultant
• 27:07
  for a while, then joined Alexion with in strategy and now at our
• 27:09
  Venice. So I'm and, and now having
• 27:12
  become the CEO, I'm really interested in other scientists,
• 27:14
  CEOs. So we would, for me, it would
• 27:16
  have to be someone like Len Schleifer from Regeneron or John
• 27:19
  Moraganor from El Nilam. People who started as
• 27:22
  scientists, built really successful companies, showed
• 27:26
  really strong perseverance over the years and commitment to what
• 27:29
  they believed was the right thing to do for their companies.
• 27:31
  And both of them, you know, had some pretty serious strategic
• 27:35
  shifts over time, especially John, right.
• 27:38
  So I think that as we go through the, the pivot that really
• 27:42
  we're, I feel like we're completing at our Venice from a
• 27:45
  company that was getting ready to launch commercially to
• 27:48
  saying, Nope, we're going to go back to phase one and focus on
• 27:50
  driving value with those assets. I'd love to sit down with those
• 27:53
  guys and talk about their learnings over the years and
• 27:56
  talk about how they've brought the scientific mind to, you
• 28:00
  know, moving forward, both very successfully on the science
• 28:03
  front and very successfully on the business front.
• 28:06
  I, I, I think having taken this role on I'm, I'm really
• 28:08
  interested in how I can bring both aspects of my background to
• 28:12
  make the company as good as it can be and really provide
• 28:16
  leadership to the great team that we already have here.
• 28:18
  So I'd love to talk to those guys and see what their
• 28:20
  learnings are. Fortunately, neither 1 is too
• 28:22
  shy. We've got a lot of information,
• 28:25
  so I maybe I'll get to do that at some point, But I, I'd love
• 28:28
  that, yeah. But look of ethics is going to
• 28:31
  get in more involved with hosting events.
• 28:33
  Maybe we can make that happen, you know, get a couple of other
• 28:36
  heads involved. I could have said living or
• 28:39
  dead, but let's, let's do aspirational, let's talk to
• 28:42
  people who are here. That sounds good to me.
• 28:45
  Yeah, I can help you with that for sure.
• 28:48
  Well, look, thank you so much for coming on, Randy.
• 28:50
  It's absolute pleasure. Well, great.
• 28:52
  Thank you very much, Max. We really appreciate the time.
• 28:55
  And please everyone like and subscribe to the Biohub and, and
• 28:58
  thank you so much. Again, thanks very much.