Latest / The BioHub - by Avetix / Episode 214 - David Crean - CBO at MediciNova

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Episode 214 - David Crean - CBO at MediciNova · The BioHub - by Avetix

• 0:06
  Welcome back to another episode of the Biohub podcast by Avetix.
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  Today I'm joined by Doctor David Crean, Chief Business Officer at
• 0:15
  Medicinova. Now.
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  David has spent more than 30 years across the life sciences
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  industry with a career spanning biotech, pharma, M and a
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  partnering venture capital, private equity and investment
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  banking. He brings a rare combination of
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  scientific depth and transaction experience from a background
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  perspective. He has a PhD in Biophysics, a
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  Masters in Oncology, and an MBA in Finance and has evaluated
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  biotech assets from almost every angle as an operator, advisor,
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  investor, and deal maker with a particular depth across
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  neurology and CNS. At Medicinova, David is helping
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  guide the company through an important period as they advance
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  MN166IN, ALS and other neurodegenerative conditions.
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  Today's conversation will discuss David's career across
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  science and deal making, the story behind Medissa Nova, the
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  opportunity within ALS, and how he thinks about business
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  development in the neuroscience market that appears to be
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  attracting renewed attention from Big Pharma.
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  David, it's a pleasure to have you with me today.
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  Thank you, Benjamin. I appreciate you inviting me
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  onto your podcast. Yeah.
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  Thanks so much. It's a, it's a pleasure.
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  But look, yeah, you spent more than 30 years across pharma,
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  biotech, M and a venture, private equity, investment
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  banking. What essentially originally
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  pulled you towards the business side of life sciences and how
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  the experiences that you've had over the past 30 years shaped
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  how you evaluate opportunities today?
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  Yeah. Thanks, Benjamin.
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  I appreciate the question. I get asked of me quite often
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  just because I do a lot of advising in the space with, with
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  entrepreneurs and trying to translate everything I've
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  learned. You know, I came to this
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  initially from the science side first as you mentioned about my
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  background was planning to go on to the, you know that to the
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  research and development side 1st.
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  And what told me towards the business side of medicine where
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  I went into business development, corporate
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  development, ultimately into you know, partnering and mergers and
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  acquisitions is what drew me into that because I didn't
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  really see myself as a lab rat, right, Being stuck in the R&D
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  labs. I saw it, my mindset was more
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  commercially driven and what sort of the, the, what
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  magnetized me towards the business side of pharma medicine
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  was the hard truth that I saw early on in my career that a
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  brilliant science or a brilliant molecule can be just what it is
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  brilliant. But it, it sometimes never gets
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  finance or does, doesn't find a partnership or commercialization
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  that actually helps a patient out.
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  So it's, it's almost that's where the science dies.
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  And so the science is necessary, yes, but it's sometimes it dies
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  and it's not sufficient. You have to be able to, you
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  know, translate that science, those great programs into, you
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  know, seeking out capital. And that's where I saw this
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  translation die. And so I wanted to make sure
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  that I had an an opportunity in my career to certainly make
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  greater impact on that. So great programs die because of
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  a lack of capital. They're not able to attract, you
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  know, capital investment from investors.
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  And, you know, that's, that's how I got to really look at a
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  number of opportunities to evaluate.
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  So I, I try not to lead with the story.
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  I lead with the biology, the strength of the data, the
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  quality of the team and whether there's really truly a realistic
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  path to value. And that and value means, you
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  know, a liquidity, it could mean an approval, it could be a
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  partnership or it could be an exit.
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  And so one of the things I've truly learned as 30, more than
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  30 years teaches you humility, if you will, about risk, about
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  risk and discipline, and then about where value actually gets
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  created in pharma. Yeah.
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  And let's let's sort of take a jump to where you are now.
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  I mean, you know, Medicinova is a fairly unusual company, if I
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  say so myself. You know, you're dual listed in
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  both Tokyo and the US, You are founded by a Japanese CEO and
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  you currently operate with a very lean model that's split
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  between San Diego and Tokyo. How would you give a brief
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  introduction to the people who you know don't yet know the
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  story? Yeah, it's great.
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  Great question and one that I deal with quite often in dealing
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  with investors, whether institutional investors, high
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  net worth, family offices, hedge funds, what have you.
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  You know, Medicinova is a clinical stage biopharma company
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  that looks small on paper from its valuation.
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  If you know where our valuation is published every day in, in in
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  NASDAQ and in Tokyo in terms of what what the value is worth our
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  market cap, but it certainly punches well above its weight.
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  I think it's an underappreciated and undervalued story.
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  We're dual listed on NASDAQ in in the United States under the
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  symbol MNOV. We're also listed on the Tokyo
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  Stock Exchange under the code 4875.
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  And you know, as you mentioned, we're, we're founded by Doctor
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  Yuichi Iwaki, Japanese physician and we have this deliberately
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  lean operation for the for the company.
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  We're spending about 12 to $13 million annually.
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  I didn't say quarterly or monthly, I said annually.
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  So you know, that's it, that's a little over about $1,000,000 a
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  month that we're we're spending. So very lean and the model is
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  really built for this capital, capital efficiency.
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  You have a small internal team, we outsource development and and
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  our infrastructure externally and we have a portfolio focused
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  on advancing clinically validated molecules with well
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  understood safety. We have two molecules MN 166
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  which you mentioned and MN001. But for the sake of today, our
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  lead asset really MN 166, which we call ibudalast is a drug that
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  has decades of human safety data outside of the United States in,
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  in Japan, in fact, that's spending more than 3,000,000
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  patients for other indications. And we're using that we're
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  exploring that that compound to advance it into treating serious
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  neurodegenerative and inflammatory diseases.
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  For example, in ALS we have a fully enrolled Phase 2B3
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  registrational trial in in ALS where you know, this is a rare,
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  rare disorder. We have fast track set, we'll
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  have orphan drug designation and you know, it's it's a condition
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  that's not treated very well. Yes, there's some approving
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  approved molecules, but they're modest in efficacy at best.
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  So there's really still a large clinical unmet medical need in
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  ALS. So you know overall Medicinova,
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  we're bi national, we have a shareholder focused company
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  trying to translate well characterized biology into a
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  late stage CNS program of ALS without the burn rate of a
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  typical biotech as I mentioned, you know 1212 or $13 million a
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  quarter, so very, very capital efficient, very exciting.
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  Yeah. And you mentioned that, you
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  know, N166 is being developed across both neurodegenerative
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  and inflammatory conditions. Can can you just sort of
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  simplify down the biology and why essentially targeting
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  neuroinflammation, glial activation and neuroprotection
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  makes sense within ALS? Yeah, so I Buddha last for MN
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  166 is a anti-inflammatory. It's a oral small molecule that
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  works inside the brain and also at the spinal cord level.
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  And it really does mainly 2 things.
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  One, it inhibits phosphodiesterate 341011 so it
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  inhibits that and it suppresses A cytokine called MIF, which is
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  macrophage migratory inhibitory factor.
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  And practically what what that does.
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  So it's got this multi mechanism of of of of mechanism of action.
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  And practically by doing that it calms over any or over activated
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  glial cells, for example microglia and astrocytes that
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  are meant to protect neurons. But in ALS the biology is that
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  these turn chronically inflamed and start doing a lot of the
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  harm. And so you start getting a build
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  up of toxic proteins. So really why does that matter
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  here? Because what we've learned in
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  ALS it's, it isn't just purely a motor neuron autonomous disease,
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  very heterogeneic. There's a lot of things going on
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  with the biology. So what what what I would say is
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  neuro inflammation and glial activation are drivers of how
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  fast motor neurons die. ALS is a motor neuron disease.
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  And so you know, neuro inflammation, glial activation,
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  big drivers. So if you can, if you will calm
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  or dial down that toxic inflammatory environment, you
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  give neurons a more protective place to live.
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  And that's, that's really the thesis.
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  It's about neural protection. And by changing the, the
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  neighborhood that the neurons operate on, not just the neuron
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  itself, but it's, you know, the sort of the whole ecosystem
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  where it lives. And so that's why we're excited
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  and why we believe it's very, very differentiated when you
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  start looking at the ALS, you know, competitive landscape.
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  Yeah. And the phase, the Phase 2B3
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  trial that you mentioned is now fully enrolled.
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  Your top line data is expected sort of towards the end of this
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  year, start of next year. What essentially makes this such
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  an important readout? But both.
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  Both for you as a company, but the broader ALS field.
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  Yeah, thank you for mentioning those.
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  This is the probably the company's most important
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  catalyst in its history and it's been around for 26 years and it
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  lands at a time when the ALS community really badly needs a
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  win or at least, you know, some positive sort of data to come
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  out. ALS itself as a as an indication
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  has had very fuse disease modifying sex sexes.
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  They've had one high profile approval of about 2 1/2 three
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  years ago called Relvio. But unfortunately when that was
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  from a company Amelix, when they had to go back and do a
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  confirmatory phase three trial, it was it failed and it was
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  pulled from the market in 2024 because of that failure in the
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  confirmatory trial. And what that did was it raised
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  the bar for everyone who is developing drugs in this area of
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  of ALS where you have a lot of the regulatory agencies, whether
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  it's on in the European side, Canadian side or US side.
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  And this has put a lot of tailwinds behind companies,
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  development programs raise the bar.
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  Combat, as you mentioned that our Combat Phase 2B3 trial is
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  fully enrolled. We fully enrolled that in
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  September of 2025 data comes. So our last patient out from
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  that trial will be in in September and by the time we
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  clean, clean up the database, lock it, it's going to be around
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  December of this year as you mentioned.
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  So for Medicine Nova, a positive result is potentially
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  transformational. It's it's, it's really a
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  difference between an early value, you know, clinical
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  company and one holding a late stage partnerable CNS asset.
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  So and then for the field and for the ALS community and
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  patients and advocates, Ibutalas or MN 166 really represents A
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  distinct mechanism of action neuroinformation, neural
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  protection in a disease in which where where most patients have
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  limited treatment options. So if we get a clean positive
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  data readout, even on a sub analysis of patient population
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  that have been enrolled, it would it it would validate the
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  the glial activation inflammatory thesis broadly, not
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  just our molecule. And it would give patients, you
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  know, at least some, some hope that we can help them from a
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  therapeutic standpoint. And and the combat trial is
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  using the combined assessment of both function and survival as
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  the primary endpoint with secondary measures including
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  ALSFRSR, muscle strength and quality of life.
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  What does a pressing ALS data set need to show today to
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  matter, You know, clinically, regulatory and also
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  commercially? Great question.
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  This is a sort of a standard regulatory, you know, endpoint
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  clinically, you need to have a real effect on function and
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  that's why our primary endpoint is the combined assessment of
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  functionality and survival, which and it's a it's a it's a
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  Co primary, which jointly ranks how patients do on a function
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  and whether they're alive. At the end of the day, it's a
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  tougher, more honest endpoint and and very high regulatory
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  standard than just functionality alone.
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  So function and survival and you know, at the end of the day, you
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  want to keep, you know, monitor this ALSFRS progression.
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  You also need to, as you mentioned, measure muscle
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  strength by denometry and also quality of life.
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  And you have to make sure that all those the primaries in the
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  secondary are all moving in the same direction.
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  So, you know, at the end of the day, for a regulator, internal
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  consistency is what's going to convince skeptics and, and the
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  regulators, the FDA and the EMEA on in the European side, they
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  want clear statistically significant robust effects on
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  something that's going to really matter to patients.
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  And ideally also, you know, reinforced by biomarkers like
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  neurofilment, lighter NFL commercially.
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  So that's regulatory commercially you, you need an
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  effect size or that's really going to make a difference for,
• 15:59
  for patients and for advocates and, and for clinicians.
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  You know, safety is obviously a very important part A and then
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  having a dosing profile or a target product profile that
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  physicians and payers are actually going to accept and
• 16:16
  adopt and cover. And so any type of marginal
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  signal in this area won't really clear the regular the
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  reimbursement bar cleanly. There might be some negotiations
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  around it, but you know, you definitely want to make sure
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  that you have, you know, clear signal in a patient population
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  or even a sub type of analysis where there it's going to the
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  signal is going to clear the reimbursement bar.
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  And you know, so right now the gold standard is when function
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  survival and biomarkers Alltel 1 coherent story and very in a
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  very consistent manner. Yeah.
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  And you've also got an NIH and NINDS supported expanded access
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  study in later stage ALS patients and that includes, as
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  you mentioned, you know neurofilament light and clinical
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  measures. How do you think about the role
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  of real world expanded access and biomarker data alongside A
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  controlled pivotal trial? Great, great question.
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  And I'm asked by investors quite quite often like how does our
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  combat ALS phase 2B registration slash 3 registrational trial,
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  How does that wrap into this other trial that we have going
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  on? And it's it's called an A
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  Synovie expanded access trial. It's in later stage ALS patients
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  and it's not a part of the registration, but collecting
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  real world evidence and biomarker data is super
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  important. So what I would say is they play
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  very complementary, very different but complementary
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  roles. And 1, I don't think you should
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  confuse that one's registration. The other one is collecting real
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  world evidence. And you know, the combat phase
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  2B3 is controlled pivotal trial, it's randomized, double-blind,
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  placebo-controlled and that is what proves causation or you
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  know what, what the regulators are going to be looking at.
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  That's evidence that the regulators are proven
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  absolutely, full stop. What the expanded access
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  biomarker work does is add texture, if you will around
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  that. It's it's adding complementary
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  information to that. And so we're in that particular
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  study, we're capturing NFL or neurofilm at light plus some
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  clinical measures and later stage real world patients.
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  Those are later stage our registrational trials actually
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  in early stage patients. So this is in later stage and
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  these are, you know, patients frankly, who generally wouldn't
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  qualify for a tighter pivotal trial just given their their
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  advanced disease. So what that does is 3 things.
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  It gives access to patients who need it super important.
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  It builds a real world safety and biomarker database and it
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  can also reinforce the regulatory and commercial story
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  on breath and and durability. So super important, you know, at
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  the end of the day, I would say and how what I message to
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  investors is the expanded access data that we're collecting in
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  later stage patients supports the pivotal trial, but it
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  doesn't substitute for it because that's in a very
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  different patient population. Yeah.
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  I mean, if we combine sort of the look of how medicine over
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  structured alongside this pivotal started.
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  I mean, you know, your your model is very capital efficient.
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  You've got a small internal team, you outsource development,
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  a lot of you know, sort of clear intention also to partner rather
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  than to build a full commercial organization.
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  Essentially, what are the advantages and the limitations
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  of this model when you are sitting on a real potential late
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  stage CNS asset? Yeah, I did.
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  I, I, I always try to come up with disadvantages, but to me
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  the advantages are it's look at, at the end of the day, it's
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  about discipline. You know, we need, we need to be
• 20:24
  good stewards of capital. So we have a small internal team
• 20:28
  with outsource research and development, which means lower
• 20:32
  fixed costs, real flexibility and, and at the end of the day
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  for importantly for investors, it's minimal dilution per
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  program. You're, I'm not carrying a 300
• 20:42
  person organization. We have 9 full time equivalents.
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  So right there, you know, for shareholder that's an efficient
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  way of using money. As I mentioned, we're you know
• 20:52
  good stewards of capital and it's about efficiency and the
• 20:57
  risks adjusted exposure to a late stage clinical asset is
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  certainly something that's very, very important.
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  Perhaps the limitation or you mentioned disadvantage is, you
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  know, let's say it's equally honest.
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  When you're sitting on a potentially late stage CN asset,
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  you don't have the internal commercial engine, if you will,
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  the sale, the sales force, the medical affairs footprint, the
• 21:22
  payer infrastructure to launch it yourself.
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  And we've made the deliberate decision not to be a commercial
• 21:29
  organization. It's, it's very, very expensive
• 21:32
  to build a sales force, a commercial infrastructure.
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  So you know, we're going to be, our intention is to partner, not
• 21:42
  to build a commercial organization.
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  So that's super important. But it, you know, it also means
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  that we still need to capture the value of this moment of the
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  data coming out at the end of the at the end of the year,
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  depending on that data and then executing a, a deal, a
• 22:00
  partnering deal with a commercial organization in this
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  space on very good terms. So the model itself, we talked
• 22:10
  about discipline and then its limitation.
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  The model optimizes for getting to the data efficiently and the
• 22:17
  discipline then has the has to, you know, you have to shift to
• 22:22
  running a competitive, well timed partnering process once
• 22:26
  the data is in hand. And that frankly is falling on
• 22:28
  me to do that as Chief Business Officer.
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  Let's let's take a step back then.
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  I mean, I know I mentioned in the introduction that a lot of
• 22:36
  your expertise and focus has been on from the broader
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  neuroscience market and big pharma interest seems to be
• 22:42
  back, you know, especially where the assets are slightly more de
• 22:46
  risked From a business development perspective, what
• 22:49
  are pharma companies looking for now in CNS that they may not
• 22:54
  have been willing to underwrite, you know, let's say 5 or even 10
• 22:57
  years ago? Yeah, I think the mood is
• 23:00
  generally genuinely changed. You saw a number of big pharmas
• 23:06
  exit and then now they're they're coming back in.
• 23:10
  They retreated from neuroscience because of, you know, because of
• 23:13
  the failure rates, the expensive failure rates and points that
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  they didn't trust or understand biology that they couldn't yet
• 23:24
  sort of drug and and hit the targets.
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  So I think what's different now it's about de risking pharma is
• 23:31
  willing to underwrite CNS again. And neuro, neuro is actually one
• 23:36
  of the if you look at some of the partnering and M and A data
• 23:40
  outside of oncology. Yeah, exactly.
• 23:43
  And you know, and obese, you know, and cardio metabolic
• 23:46
  disease, obesity GOP ones all that's it.
• 23:49
  You know, CNS is is back in in favor.
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  You know, you have human proof of concept, a mechanism that
• 23:56
  they finally understand or at least understand better,
• 23:58
  especially in areas like Alzheimer's, ALS and
• 24:02
  Parkinson's, some others Huntington's disease.
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  You know, they're they're looking for their understanding
• 24:08
  the safety profile a little bit better and then bio ideally
• 24:11
  biomarkers that are starting to track outcomes and real really
• 24:15
  leading to personalized medicine.
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  You see a number of recent large CNS acquisitions, which tells
• 24:22
  you the appetite for large pharma, which have big balance
• 24:26
  sheets and they need to, you know, frankly spend money to
• 24:30
  deal with loss of exclusivity and just portfolio gaps.
• 24:35
  Look at I think it's real. They're paying for optionality
• 24:38
  on validated mechanisms without owning the early failure risk,
• 24:43
  if you will. So for a company like
• 24:45
  Medicinova, that's the whole thesis, if you will.
• 24:49
  Let's get to a partnering table with a readout or a, you know
• 24:53
  that on our fully enrolled registration of trial with a
• 24:57
  compound that has decades of safety data and a very
• 25:00
  differentiated mechanism. And that's a very different
• 25:03
  asset then let's say if we were in early stage phase one story
• 25:08
  and that's very, very, it's priced very, very differently.
• 25:12
  So I'm excited about it as we start to approach the end of
• 25:15
  the. Year, yeah, yeah, me too, that's
• 25:17
  for sure. There, there seems to be a few
• 25:20
  real big industry themes around neuroscience right now.
• 25:22
  I mean, blood brain barrier, delivery payer pressure, patient
• 25:27
  heterogeneity and AI driven child design.
• 25:31
  Which of these do you really think will most change how CNF
• 25:36
  drugs are developed and partnered over the next decade?
• 25:42
  Yeah. I think all of our all four of
• 25:45
  those areas that you mentioned are super important.
• 25:48
  The one that I'm particularly interested in watching and the
• 25:55
  sick, it's showing a great deal of excitement is on this blood
• 25:58
  brain barrier delivery and using some of this brain shuttle
• 26:02
  technology where you know a number of big pharma's in
• 26:06
  particular Roche is looking in the Alzheimer's space for
• 26:09
  example, is it's an exciting area.
• 26:13
  So drugs that are typically have not been able to get through the
• 26:18
  barrier of the blood brain barrier are now being shuttled
• 26:22
  across with some technologies. I know that Denali also has a
• 26:25
  technology that it it it, that they're pursuing as well.
• 26:29
  So that's the one that I really like to spend a lot of time on
• 26:34
  because I think it's going to fundamentally change how
• 26:37
  getting, you know, large molecules, biologics, for
• 26:40
  example, or maybe even small molecules that have the
• 26:43
  difficulty getting across the barrier getting in inside the
• 26:47
  neuron. And whether that's going after
• 26:49
  amyloid beta or Tau as relates to Alzheimer's.
• 26:54
  And then ALS same, same situation dealing dealing with
• 26:58
  like toxic proteins of TDP 43 things like that.
• 27:02
  I'm excited about that. But that doesn't mean that I
• 27:05
  dismiss or not interested in watching like payer pressure and
• 27:09
  Petter patient heterogeneity as real constraints or AI driven
• 27:15
  trial design, because they're going to make, make essentially
• 27:19
  make studies faster, smarter. You're going to have better,
• 27:23
  more, you know, homogeneous patient populations, if you
• 27:28
  will. So let's not let's not undersell
• 27:31
  that. But definitely I think from my
• 27:35
  perspective, getting the drug, these drugs to to the area of
• 27:42
  CNS where the biology is sort of misframed.
• 27:47
  I think that's super important. Get the get the drug to the
• 27:50
  right area of the brain. So that to me is, you know,
• 27:53
  certainly where I where I will and have been spending a lot of
• 27:57
  time. Yeah.
• 27:57
  And. From, from what you know, from
• 27:59
  your research, how I know this is an open-ended question, but
• 28:03
  how far really do you think we are away from a genuine
• 28:07
  breakthrough within that field that's going to ultimately
• 28:11
  change the way that we deliver, you know, drugs to the brain?
• 28:16
  Well, by, by the terminology use a breakthrough.
• 28:20
  I, I have to rely upon, you know, it being approved by
• 28:24
  Regulatory agency. So that's my a priori assumption
• 28:29
  on, you know, breakthrough. And if you use that, I think
• 28:33
  it's within, you know, a few years.
• 28:35
  Roche's, you know, Roche is checking their, their compound
• 28:40
  with the brother brain shuttle technology going after
• 28:43
  Alzheimer's, early stage of Alzheimer's in a anti amyloid
• 28:48
  beta approach. I think you're going to and
• 28:52
  they're in, you know, later stage trials are in phase three
• 28:55
  trials. So that's probably at least two
• 28:57
  to three years away. And I think there's also some
• 29:00
  people who are applying it towards, you know, going after
• 29:05
  Tau tangles and Alzheimer's. So I, I'm giving it two to three
• 29:10
  years. So a lot of a lot more people
• 29:12
  are pursuing the technology to get drugs to the right place in
• 29:18
  the brain. So yeah, that's that's kind of
• 29:22
  my timelines right now. Yes, it's certainly going to be
• 29:24
  an exciting space to watch, that's for sure.
• 29:27
  But look, just to sort of wrap things up, David, if you could
• 29:31
  have dinner with any scientist or innovator, past or present,
• 29:34
  who would it be and why? You know, I when I, you asked me
• 29:41
  this question, I think the first time we met, you asked me, hey,
• 29:45
  give it some thought. I really tried to give it some,
• 29:49
  you know, very well, deep consideration and there's three
• 29:53
  people that I love to follow, I respect, and I like what they're
• 30:00
  doing in the ecosystem. 1 is Newbar Afian from Flagship
• 30:07
  Pioneering immigrant, super smart.
• 30:10
  He was the founder of Flagship Pioneering, which is a great
• 30:13
  venture capital firm, and I think he thinks about biotech in
• 30:17
  a way that almost no one else does.
• 30:20
  He starts from the sort of the premise or the a priori
• 30:25
  assumption that, you know, what would have to be true for a
• 30:31
  company to be successful. And then he builds companies
• 30:34
  around that bold, unreasonable sort of thesis rather than
• 30:40
  incremental bets. So it's very transformative.
• 30:43
  And I think he's probably the closest thing in our industry to
• 30:48
  a a systemic inventor of of new companies of Newcos.
• 30:54
  So that's pretty cool. Secondly, also in the Boston,
• 30:57
  he's located in Boston. Secondly, also in the Boston
• 31:01
  area comes out of MIT would be Bob Langer.
• 31:06
  He's at MIT, as I mentioned, great.
• 31:09
  I mean engineer by training. He's one of the most prolific
• 31:12
  inventors in medicine. He started so many, so many
• 31:16
  Newcos have came, come out of his lab and it frankly many of
• 31:21
  those Newcos have gone on to be acquired by Big Pharma or by
• 31:27
  medical device companies. And he does a lot of work in the
• 31:29
  drug delivery space. And so he is basically seated an
• 31:33
  entire generation of therapeutics and Newcos and
• 31:36
  founders. And then lastly, and this is
• 31:39
  kind of my San Diego connection is Doctor Eric Topol, physician
• 31:45
  by by training. He's at Scripps Research
• 31:47
  Institute in San Diego and he's and he's one who I like to
• 31:52
  always see him as keeping, keeping us honest and about
• 31:55
  where medicine is actually meeting the patient, you know,
• 32:00
  whether it's on data or it's on AI or, you know, certainly going
• 32:04
  through evidence versus hype. So I think putting those three
• 32:09
  together, you know, Newbar, Bob Langer, Eric Topol, you get 3
• 32:14
  forces that really create value in the business of, of life
• 32:17
  science. And they have, they have the,
• 32:20
  you know, sort of the audacity to ask the right questions, the
• 32:24
  engineering rigor to make it real, especially with Bob
• 32:29
  Langer, and then the discipline to prove it in the, in the real
• 32:31
  world. So, you know, if I was at the
• 32:35
  dinner table, then I, I'd be listening a lot.
• 32:37
  I'm just asking a lot of questions.
• 32:39
  Yeah, and if you, if you ever managed to get that, that dinner
• 32:42
  party arranged, I'd like to hope there'd be a fifth seat that I
• 32:46
  could come and join as. Well, there you go.
• 32:49
  There you go. We'll get a table for five.
• 32:51
  Sounds perfect. Well, it's been a been an
• 32:53
  absolute pleasure to to have you join me today, David.
• 32:56
  I've really enjoyed our conversation.
• 32:57
  Thank you very much. I appreciate your time and thank
• 33:00
  you for allowing me to come on and share with your readership.
• 33:03
  Absolutely and thanks to everyone for listening or
• 33:06
  watching along and make sure you stay tuned for future episode.
• 33:09
  But that's that's it for now. Thanks and goodbye.
• 33:13
  Alright, bye, bye.