Latest / The BioHub - by Avetix / Episode 66 - Andy Parker - CEO of Step Pharma

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Episode 66 - Andy Parker - CEO of Step Pharma · The BioHub - by Avetix

• 0:06
  Welcome to another episode of the Bio Hub.
• 0:08
  Today I'm joined by Andy Parker, the CEO of Steppe Farmer, and he
• 0:13
  has spent over 2 decades in biotech and pharma, holding
• 0:17
  senior leadership roles at companies like Astra Zeneca,
• 0:19
  Shire and Zealand Pharma and even spending time on the VC
• 0:23
  time closure. Since 2019, he's been leading
• 0:27
  Steppe Farmer, a company developing first in class CTPS 1
• 0:31
  inhibitors with their lead program now in the clinic for
• 0:34
  cancer. We talk about the science behind
• 0:36
  steps, approach, what's next for the company and Andy's
• 0:39
  experience moving from big pharma to small biotech, plus
• 0:43
  lessons on fundraising in today's market and building a
• 0:46
  great work culture. It's an absolute pleasure to
• 0:49
  have you, Andy, how are you? Very good.
• 0:51
  Thanks Max for inviting me. No, it's amazing.
• 0:55
  So you've had the pretty interesting path, You know, we
• 0:59
  talked about AZ, Shire and also VC.
• 1:02
  What? What then LED you onto Steppe
• 1:04
  Farmer? Yeah, I, I think I've been very
• 1:09
  lucky to work across a broad spectrum of companies, you know,
• 1:13
  from that big pharma to the mid size and start up biotech as
• 1:17
  well as VC. So that that's been a privilege.
• 1:20
  I think I've also been very lucky to have worked across a
• 1:24
  number of different countries, which has exposed me to
• 1:27
  different ways to do things, trying to pick the best from
• 1:29
  each of those across the US, the UK, Denmark, Switzerland,
• 1:35
  etcetera. My preference having been
• 1:38
  through those experiences is clearly to be working in a small
• 1:42
  biotech environments and I was really attracted to Steppe
• 1:46
  Farmer because of the underlying mechanism to the human genetic
• 1:51
  story that validates CTPS 1 as a target.
• 1:55
  Also because there were a lot of my former AstraZeneca colleagues
• 1:59
  at Signature in Nottingham who had run all of the medicinal
• 2:04
  chemistry in the early days of the company to get to that lead
• 2:07
  candidate and a fantastic syndicate of investors who were
• 2:11
  very much behind the company. So all of those things were were
• 2:16
  really attractive when presented with the opportunity to to pick
• 2:19
  up the reins and and lead the company from 2019 onwards.
• 2:23
  Bearing in mind that the company was founded in 2015.
• 2:26
  So it had already been running for a few years and was at the
• 2:29
  point of having that clinical candidate identified by the time
• 2:32
  I came in. So I can really see a clear path
• 2:34
  forward to build a team to take the program on through Ind
• 2:39
  enabling studies and into the clinic.
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  So joined at an exciting time with a really interesting
• 2:44
  mechanism. That's awesome.
• 2:47
  And those for for people who don't know who step are what,
• 2:51
  what's the core of what you're building?
• 2:53
  So we're a French biotech company.
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  We're headquartered in Paris, but physically located in Saint
• 3:00
  Genie, which is very close to Geneva, Switzerland.
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  And we are essentially a single mechanism company.
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  So we focus on developing inhibitors of the enzyme CTP
• 3:12
  synthase One. This is a first in class
• 3:15
  approach. So nobody else out there has the
• 3:17
  CTPS 1 inhibitor close to the clinic and in fact there are not
• 3:22
  that many activities is happening preclinically.
• 3:24
  So we're really sort of trailblazing this first in class
• 3:28
  opportunity. The reason it's interesting
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  initially comes from Human Genetics.
• 3:33
  So the founding scientist Alan Fisher at the Imagine Institute
• 3:38
  identified found the population of kids in the UK that had a
• 3:43
  profound inhibition inability to fight a viral infection.
• 3:47
  When they looked at the lymphocytes in those
• 3:50
  individuals, that immune cell repertoire was perfectly normal.
• 3:54
  But when they tried to activate those cells X vivo to make them
• 3:56
  proliferate, as if they were going to mount an immune
• 3:58
  response, they wouldn't proliferate.
• 4:01
  So that explained why these kids couldn't mount the response to
• 4:05
  the viral infection. And then using genetics, they
• 4:08
  established that the cause of that phenotype was a mutation in
• 4:12
  the gene that codes for CTP synthase 1.
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  So it was essentially a a null mutation.
• 4:18
  That really taught us that if you lack CTP synthase 1, you
• 4:23
  have this profound inability for your lymphocytes to proliferate.
• 4:27
  But what was really interesting about the observation was that
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  there was nothing else wrong in these kids.
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  So every other cell type in the body, in the absence of CTPS,
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  one could actually use an orthologous enzyme called CTP
• 4:41
  synthase 2 to make their CTP. And so that was really the
• 4:44
  genesis of the company. Could we develop a truly
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  selective CTPS 1 inhibitor that would block aberrant lymphocyte
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  proliferation and enable you to then target that pathway very
• 4:57
  selectively from a lymphoma perspective?
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  And that's really how we got on to sort of develop the company
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  and enter lymphoma space as our first clinical trial.
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  But it's become much more interesting since then because I
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  would say what we've done is the genetics pointed us to this
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  phenotype around lymphocytes. But we've followed the science
• 5:20
  all the way through as we entered the clinic in 2022 and
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  began to ask ourselves questions about where else could you use
• 5:28
  this mechanism? How could you use this mechanism
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  in solid tumours? So in solid tumours, we would
• 5:34
  argue that solid tumours expressed both CTPS 1 and CTPS
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  2. Therefore, if we inhibited CTPS
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  1, they would use CTPS 2 to make their CTP.
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  So not a sensible place to play as opposed to the lymphocyte
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  population where we know CTPS 2 can't complement for the loss of
• 5:54
  CTPS one. But we asked the question are
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  there solid tumours that have deleted CTPS 2?
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  And the answer to that question is yes.
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  And there are a whole range of solid tumour types that have
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  deleted CTPS 2, which creates this absolute dependency for the
• 6:10
  tumour on CTP synthase 1. And so we've moved now towards
• 6:15
  solid tumours and we've started a clinical trial in solid
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  tumours where we select patients for the loss of CTP synthase 2.
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  And our plan right now is to focus on ovarian, endometrial
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  and lung cancer, where the prevalence of the loss of CTPS 2
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  is between 15 and 20%. So there's a high prevalence of
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  the loss of CTPS 2 in tumours. We estimate one in 10 solid
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  tumours have deleted CTPS 2. And then we've also followed the
• 6:45
  science from the lymphoma study in understanding that as we
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  dosed more and more patients through the escalation, we only
• 6:53
  have one recurrent adverse event and that is thrombocytopenia.
• 6:57
  So we have an effect on platelets and in order to
• 7:01
  mitigate that effect on platelets, we developed a
• 7:03
  schedule to dose the patients one week on drug, one week off
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  so that we mitigate that platelet drop.
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  But as we built out the data set, we realised that we did not
• 7:14
  see any other recurrent adverse events.
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  So we asked the question, could that safety signal be turned
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  into a therapeutic endpoint? And the answer is in the benign
• 7:24
  hematological condition, essential thrombocythemia, it
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  can, because this is a condition where there's an overproduction
• 7:32
  of platelets. And what you need to do is to
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  normalise platelet numbers in that patient population in order
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  to help them avoid the issues that come from elevated
• 7:43
  platelets, which is thrombotic events.
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  So now we're just about to start a study in essential
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  thrombocythemia where we'll dose the drug very differently.
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  But I think the important thing is we've really followed the
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  science. Genetics took us into the
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  lymphoproliferative space, then understanding the loss of CTPS 2
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  took us into solid tumour space and then understanding our
• 8:06
  profile for our drug took us into the ET space.
• 8:10
  So that drug is called Dencatistat.
• 8:12
  It's the first in class CTPS 1 inhibitor and it's well advanced
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  now in its phase one escalation in lymphoma and its phase one
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  escalation in solid tumours and about to start in the essential
• 8:25
  thrombocytemia space. So we aim to maintain our
• 8:28
  position as world leaders in developing CTPS 1 inhibitors
• 8:32
  primarily focused on Dencatistat as the lead asset.
• 8:36
  Yeah, it's been a cool journey so far.
• 8:38
  Like to get to the point you are now and obviously getting to the
• 8:41
  clinic was like massive milestone and what, what's next
• 8:46
  then what's the what's next for step and then what milestones
• 8:51
  are you looking at next as, as big ones?
• 8:55
  Yeah. So I would say for each of the
• 8:58
  indications, there are sort of big things coming over the next
• 9:00
  1218 months. So in the lymphoma study, we're
• 9:06
  recruiting both T&B cell lymphoma patients.
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  We just received orphan drug designation for T cell lymphoma.
• 9:13
  We'll be following that up with more regulatory interactions,
• 9:18
  most notably at end of phase one meeting with the FDA that will
• 9:21
  come sometime in the first half of next year.
• 9:25
  So moving forward then into phase two, most likely focused
• 9:29
  on T cell lymphoma in Phase 2. So peripheral and cutaneous T
• 9:33
  cell lymphoma in the solid tumour space.
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  Dose escalation has been in all comers.
• 9:39
  So by the end of this year we will be into CTPS 2 null
• 9:44
  selected patients, both lung, endometrial and ovarian.
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  So throughout the course of next year, we'll be building the
• 9:51
  clinical data to demonstrate that we have clinical activity
• 9:56
  in those patients and more importantly, to develop the
• 9:59
  concept of pan cancer opportunity for this mechanism
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  because it works in ovarian cancers that are CTPS 2 null,
• 10:08
  lung cancers that are CTPS 2 null.
• 10:10
  It should work in any cancer where you can determine that
• 10:13
  they are CTPS 2 null. So in the end, we'll be looking
• 10:16
  for that tumour agnostic approval.
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  But throughout the course of next year, that data set will
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  come and confirm the hypothesis and build out that pan cancer
• 10:25
  opportunity. And then in essential
• 10:27
  thrombocythemia, we will start dosing patients in the next few
• 10:30
  weeks and we will get a very quick proof of concept there
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  because what we're looking for is platelet numbers to be
• 10:36
  normalised. And so it's a relatively simple
• 10:39
  readout. We expect the effects to come on
• 10:42
  pretty quickly. So probably in the next 6 to 9
• 10:45
  months, we'll start to understand whether we have a
• 10:47
  good drug for ET in our hands. So there's a lot coming over the
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  next 12 to 18 months in terms of demonstrating proof of concept
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  in multiple indications. That's amazing.
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  That's so cool. So when you look at like the big
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  picture for step, like what, what's the long term goal?
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  What? What do you want step to become?
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  I think we have to ensure that we maintain our leadership
• 11:16
  targeting CTPS 1. And then I think the most
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  important thing is that we are efficient in running our
• 11:25
  clinical studies to as quickly as possible demonstrate the
• 11:28
  benefit to patients in hard to treat cancers.
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  And maybe most importantly build out the organization to enable
• 11:36
  us to do that. But also find in the long term,
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  the right partner that can actually realise the ambition
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  here, which is to develop this drug across multiple cancer
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  types and potentially as a pan cancer therapeutic in the solid
• 11:49
  tumour space. And I'm conscious that that is
• 11:52
  likely to require us to have partners to do that.
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  Partners to help us with the development of the companion
• 11:59
  diagnostic that would run alongside this, partners to help
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  us with financing the breadth of activities that would need to be
• 12:07
  undertaken to demonstrate the pan cancer potential here.
• 12:11
  So I think that that that that's the key.
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  It's let's grow the company to deliver on the phase twos and
• 12:17
  then let's be mindful of how we're going to really manage
• 12:20
  this to expand enormously in the phase three setting in the long
• 12:24
  run. Yeah.
• 12:26
  Nice. And are you looking at like
• 12:28
  those partnerships now for the future and like evaluating, is
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  that how early you look at it? I think we're always talking to
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  people about opportunities. I think we are still at a point
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  now where we need to firm up on the data set to really
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  demonstrate that the hypothesis we have around the solid tumors
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  and around the ET hold true. And then I think the opportunity
• 12:52
  to partner will become much more straightforward as we move on.
• 12:57
  Yeah. And then rather than the deal
• 13:00
  making side, like everyone knows industry is pretty tough at the
• 13:04
  moment and fundraising is, I mean, pretty brutal.
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  How have you approached it and what and what's been key to
• 13:14
  getting these fundraise over the line?
• 13:18
  Yeah. So we, we, we're in a Series C
• 13:21
  financing mode right now. We're hoping that we'll close
• 13:24
  that round out before the end of the year.
• 13:26
  We're making very good progress. I think the key to making
• 13:30
  progress is really the clarity of the science, the clarity of
• 13:36
  the messaging around the value inflection points that will be
• 13:39
  delivered through that financing that's being proposed.
• 13:45
  And then if you have good insider support, then that's
• 13:49
  significantly eases the conversations that you're going
• 13:53
  to have with people around trying to raise money.
• 13:58
  And then persistence, I think that's also important.
• 14:02
  A no invariably doesn't really mean no.
• 14:06
  So the number of people that I have talked to where a no
• 14:10
  initially, when you continue to update them, continue to bring
• 14:14
  new data, etcetera, moves from a no to a maybe.
• 14:19
  And then with the very few, ultimately you convert those
• 14:22
  maybes into a yes. So I think you have to be
• 14:25
  persistent. This is it's a long game in
• 14:28
  terms of fundraising. You have to talk to an awful lot
• 14:31
  of people. You have to build a lot of
• 14:32
  relationships and you have to accept that no doesn't really
• 14:37
  always mean no. So I think that's that's key
• 14:41
  because it takes a long time, particularly in this climate, to
• 14:45
  actually close the financial round.
• 14:48
  So, yeah, my only advice would be don't give up, don't get
• 14:54
  despondent around the nose, keep going back, keep the
• 14:57
  relationship strong because those nose will convert over
• 15:00
  time, especially as data matures.
• 15:03
  I think it's probably much more difficult if you're a
• 15:05
  preclinical company. But as a clinical company for
• 15:08
  us, as the data has matured over the course of the last 6 and 12
• 15:13
  months, those conversations have very definitely moved from nose
• 15:16
  to maybes and in some cases to yes.
• 15:20
  And as I say, we hope that we'll close the round out and be
• 15:22
  finished with this financing effort by the end of the year.
• 15:28
  Amazing. And do you think you might put
• 15:31
  you on the spot here a little bit, but in terms of the market,
• 15:33
  do you think it's changing, getting better?
• 15:38
  I think it's always difficult. I think it's been, if I reflect
• 15:42
  back on the last round, it was easier to raise money four years
• 15:48
  ago than it is now. It has taken me a lot longer.
• 15:53
  It has required an interaction with many more funds.
• 15:57
  So I think it is a tough environment right now.
• 16:00
  I think that, you know, fads change, people move in terms of
• 16:05
  the things that they're looking for.
• 16:07
  Oncology particularly is now much more difficult because of
• 16:11
  the the plethora of opportunities there are to
• 16:13
  invest in. So trying to find and
• 16:16
  demonstrate the differentiation you have compared to others.
• 16:19
  For instance, us being first in class is definitely a positive
• 16:23
  and trying to show that you de risk is going to be key.
• 16:27
  So again for us having three shots on goal with three
• 16:30
  different indications is quite different from a binary
• 16:33
  opportunity 1 molecule 1 indication.
• 16:37
  So all of those things I think investors are are looking for.
• 16:40
  But yeah, it's it's not easy and I'm not sure it's going to get
• 16:43
  any easier quickly right now. Yeah, Yeah.
• 16:48
  Unfortunately, that's kind of what I'm seeing as well as
• 16:52
  there's just so many uncertainties, right like in the
• 16:56
  market and people just don't necessarily know which which
• 16:59
  ways to go. So one of the key, one of the
• 17:02
  main phrases I keep hearing is data is, is key.
• 17:05
  Like you, you just said it then you know, it's easy being a
• 17:08
  clinical company, you know, you can back up your results and
• 17:13
  without being too brutal. But I suppose there was too many
• 17:15
  mistakes in that like 2020-2021 period where investors put big
• 17:21
  rounds in and they didn't come to fruition.
• 17:24
  So then they're more cautious and then there's a political
• 17:28
  environment that's a bit unstable.
• 17:30
  And you know, it's there's just a few factors that have just
• 17:34
  aligned right. Yeah.
• 17:36
  I think there are a lot of platform companies that people
• 17:39
  invested in based primarily on preclinical early data that
• 17:43
  didn't pan out. So that has burnt some people I
• 17:46
  think in the oncology space and and in and in other areas, you
• 17:51
  know, small molecules seem to be not in trend.
• 17:55
  Although I think it's also important to remember that small
• 17:57
  molecules still are a massive component of approved drugs that
• 18:01
  are a massive component of drugs in clinical development
• 18:04
  pipelines. But in oncology, you can see the
• 18:07
  fad towards ADC's and towards radio ligands and away from
• 18:14
  small molecules. So I'm always keen to emphasize
• 18:17
  that, you know, there are many benefits to a small molecule as
• 18:21
  a drug versus going after an antibody as an ADC or antibody
• 18:25
  or peptide as a radio ligand. You know, we're cheap to make,
• 18:28
  we're convenient to take. And if we get the, the, the, the
• 18:32
  molecule right, then you've got a very specific and selective
• 18:35
  approach to target any element of biology, in our case tumors,
• 18:40
  but in other cases, you know, in the autoimmune space and CNS
• 18:43
  etcetera, you still have that. So let's not forget small
• 18:47
  molecules, even though the the trend right now is to go for,
• 18:51
  you know, the directions. Yeah, definitely, definitely.
• 18:55
  It's these trends are funny. I always think that like a
• 19:00
  modality can go from hero to 0 so quickly.
• 19:05
  For example, like cell therapy, like everyone was on it and
• 19:09
  there was so many big private races in cell therapy and like
• 19:12
  no one wants to even touch it now.
• 19:14
  Even from a recruitment standpoint, everyone, every
• 19:18
  candidate wanted to be involved in cell therapy, even if they
• 19:21
  hadn't necessarily had the experience before, which you get
• 19:23
  away with because it was a relatively new field, but now
• 19:27
  it's just gone the complete opposite way.
• 19:29
  It's crazy how it can literally go and these and the VCs kind of
• 19:35
  follow these trends a lot. Yeah.
• 19:39
  I mean CAR T has been an area where there's been significant
• 19:42
  investment in, in oncology. It's certainly shown significant
• 19:48
  benefit in certain instances. So there are some diseases where
• 19:53
  Karti is really having huge impact, but there are others
• 19:56
  where it hasn't been as successful.
• 19:58
  I think people forget that there is quite a significant relapse
• 20:03
  rate following Karti. And you've also still got to
• 20:06
  deal with the cytokine issues that go with treating patients.
• 20:09
  So whilst in certain situations it's a fantastic curative
• 20:14
  therapy, in many other situations it hasn't quite
• 20:18
  delivered that. And then there's the expense of
• 20:21
  treating people with cell therapies versus conventional
• 20:24
  therapies from antibodies to small molecules.
• 20:27
  It's quite, it's quite a different business model.
• 20:30
  I mean, the same is true of gene therapy.
• 20:31
  Not an area I know very much about, but it's, you know, it's
• 20:33
  similar in terms of the huge expense to treat.
• 20:38
  So you've got some economic arguments you have to win there
• 20:41
  as well. Yeah, and there's some there's
• 20:44
  some interesting companies that kind of counteract that, you
• 20:47
  know, they're looking at the cost and and trying to bring it
• 20:50
  down. Sorry, we've gone massively off
• 20:51
  track, but yeah, I'm going to completely change the the
• 20:56
  subject now. And I, I want to talk about like
• 21:00
  work environment, like how do you create a great work
• 21:03
  environment, especially for a small, dynamic, ambitious team
• 21:08
  as well? Yeah.
• 21:10
  I, I, I think for a small biotech company setting and, and
• 21:16
  particularly like us, where we really started to grow the
• 21:18
  company during COVID and, and for at least a year and a half,
• 21:23
  we're hiring people by video. We're running the company by
• 21:26
  video. It's really important to think
• 21:30
  very carefully when you hire people because a small company
• 21:35
  of 8/10/12 people is essentially a small family.
• 21:40
  So I've written very careful to focus on bringing people in with
• 21:44
  the right experience, with the right competencies, but also
• 21:48
  making sure that we have the right cultural fit so that we
• 21:52
  don't have anybody who essentially disrupts the car
• 21:56
  when the number of people involved in the company is
• 21:58
  actually that small. You know, I think it's different
• 22:01
  in much bigger organisations, but I think for a small biotech
• 22:05
  company, you know, especially if you're going to run it semi
• 22:07
  virtually, you're going to meet together as a team infrequently.
• 22:12
  I mean, we meet together as a team every other week for three
• 22:15
  days. So it's not that we're in the
• 22:17
  office all the time with each other and 70% of the time we're
• 22:20
  interacting by video. So you need to know that
• 22:24
  everyone can work like that, but but also that when we are
• 22:28
  together, it's actually a great feel that we've got the right
• 22:31
  respect, we've got the right listening and we've empowered
• 22:34
  everybody so that they know what they're doing, that they're free
• 22:38
  to do it and get on with it. The need to be referring back.
• 22:42
  I think that's that's the way that you get a small biotech
• 22:44
  company to function effectively. I think if we were much bigger
• 22:48
  and you had everybody in the office and you had labs, it's
• 22:52
  quite different, you know, and that would reflect back on past
• 22:55
  experiences in in bigger organisations which wouldn't
• 22:58
  work the way that in a small semi virtual organisations work.
• 23:02
  So it's all about people in the dynamics of people as well as
• 23:06
  their experience, their background, what they bring in
• 23:08
  terms of competency. I yeah, I couldn't agree more.
• 23:12
  And I suppose the hard thing is that is how do you check for for
• 23:16
  those kind of like personality fits for you?
• 23:20
  Is it is it off like gut feeling and just conversations with
• 23:25
  them? Would you go deeper?
• 23:27
  I think you get a good feel in the 1st 10 minutes when you're
• 23:30
  talking to somebody and and then you start to delve deeper into
• 23:36
  not so much their personality because all of that comes out as
• 23:40
  you have more conversations. So you start delving into the
• 23:42
  scientific background or their clinical experience or
• 23:45
  regulatory experience, et cetera.
• 23:47
  And then their personalities show through in what they're
• 23:50
  talking about and you begin to form an opinion of, okay, is
• 23:52
  this person going to fit into the team?
• 23:55
  You know, do I believe that that to be the case?
• 23:58
  So yeah, I think it's it's a little bit of gut feeling and
• 24:01
  just picking things up as you go.
• 24:03
  I mean, interview processes take time.
• 24:05
  So you've multiple rounds of interaction before you finally,
• 24:08
  you know, offer somebody a role and you've worked it out by
• 24:11
  then. Yeah.
• 24:12
  And that's that's definitely something you get better at
• 24:15
  throughout your career. Like everyone's made bad hires.
• 24:21
  There's they're in jail and then you learn from there and so on.
• 24:24
  So yeah, it's just something you improving, right?
• 24:27
  Yeah, COVID taught us actually how to be, how to be much better
• 24:32
  at assessing people down a video screen because we had to,
• 24:36
  because we couldn't meet people. And I hired a couple of key
• 24:39
  individuals into the company through that period, all based
• 24:42
  on video interactions. You had actually then turned out
• 24:45
  to be exactly the people I expected them to be when I met
• 24:48
  them in person. But the same is true of raising
• 24:51
  money. I raised money through COVID and
• 24:53
  had investors that I never met face to face, which is almost
• 24:56
  unheard of to to actually not be in a room, shake someone's hand,
• 25:00
  look them in the eye. So I think COVID really taught
• 25:03
  us, you know, how to better use video to evaluate people and
• 25:07
  understand people than previously when we weren't so
• 25:10
  dependent upon Zoom and Teams and other formats.
• 25:15
  Yeah, yeah, I agree. And it's it's proven that, you
• 25:19
  know, if you if, if we couldn't do our job from anywhere in the
• 25:22
  world before, like you definitely can.
• 25:26
  And like from a recruitment standpoint like that, that then
• 25:29
  opens up the amount of people you can then talk to and the
• 25:34
  pool of individuals that then that fit that position.
• 25:36
  So, you know, you can even afford to be that little bit
• 25:39
  more picky in terms of the profiles you bring in.
• 25:41
  So yeah, I agree with that so much.
• 25:45
  Our final question, which is a question we ask every guest that
• 25:49
  comes on the podcast, which is if you could be sat next to
• 25:54
  anyone at a dinner party and this person can be dead or
• 25:58
  alive, who, who would it be and why I.
• 26:03
  Mean there's so many people you could you could want to sit next
• 26:06
  to a dinner party. I guess I'm reading reading a
• 26:10
  book at the moment by Jim Watson.
• 26:13
  So I think maybe he would be a really interesting person to sit
• 26:17
  next to at a dinner party. I think to talk through that
• 26:22
  initial sort of solving of the structure of DNA through to
• 26:25
  everything that's gone on in one lifetime in, in molecular
• 26:29
  biology and the role that he's played there, because he's done
• 26:32
  an awful lot of things along the way beyond the early stuff that
• 26:37
  was that was done around solving that structure.
• 26:40
  So I think he would be a fascinating person to sit next
• 26:43
  to. But, but, but I think on a, on a
• 26:45
  more personal note, a person that I would actually love to
• 26:49
  sit down with is actually my old biology teacher, because I had
• 26:54
  this fantastic biology teacher at school who got me into
• 26:58
  science, led me all the way through then to what, what I've
• 27:02
  done now. And I haven't seen him since I
• 27:04
  left school. His name is Jake Cremona and I,
• 27:06
  I'd love to actually sit down next to him because he'd have
• 27:11
  lots of stories to tell about other students that came through
• 27:14
  after me. And I think that'd, that'd be
• 27:16
  fascinating as well. So that's a more personal touch
• 27:18
  of somebody that I'd love to sit down next to.
• 27:20
  And I'm not even sure if he's still alive, but you know that
• 27:23
  that would be great as well. That's such a cool answer.
• 27:26
  I love that, you know, someone who kind of shaped what you
• 27:29
  wanted to go into and all of that.
• 27:31
  Yeah, amazing. It's been an absolute pleasure
• 27:34
  to have you on, Andy. No, it's been a pleasure, Max.
• 27:38
  Great to speak with you. Yeah, and everyone please like
• 27:40
  and subscribe to the Bio Hub and thanks so much again, Andy.
• 27:44
  Great. You're welcome.
• 27:45
  All right.