TRANSCRIPT
Welcome To The Chain
Announcement
Welcome
to
The
Chain,
the
podcast
exploring
the
lives,
careers,
research,
and
discoveries
of
protein
engineers,
scientists,
and
biotech
professionals.
We
look
at
the
impact
their
work
is
having
on
the
field
and
where
the
industry
is
headed.
Tune
in
to
stay
up
to
date
on
the
newest
advancements
and
to
hear
the
stories
that
are
impacting
the
world
of
biologics.
Meet Jack Elands And Adcytherix
Rakesh Dixit
All
right,
so
good
morning,
everyone,
and
good
afternoon
in
Europe.
My
name
is
Rakesh
Dixit.
I'm
a
toxicologist
and
translational
drug
development
scientist
with
you
know
multiple
years
of
experience
over
35
years
in
biologics,
ADCs,
biospecifics,
peptides,
and
all
the
advanced
therapeutic
platform.
You
know,
in
my
previous
role
at
AstroZeneca
and
at
J&J
and
Medimmune
Company,
I
have
been
actively
involved
in
in
multiple
areas,
biologics
RD
and
small
molecule
drug
development.
Enough
about
me,
but
in
this
podcast,
I'll
be
speaking
with
the
leaders
across
biotechnology.
And
and
with
that
one,
I'm
so
delighted
today
to
welcome
Dr.
Jack
Elands.
Jack
is
a
founder
and
CEO
of
Adcythrix,
a
next
generation
ADC
company
that
is
focused
on
developing
highly
differentiated
ADCs
for
cancer
and
other
diseases
with
high
end
medical
need.
Very
quick
about
Jack.
Jack
is
a
highly
experienced
biotech
entrepreneur
and
ADC
leader,
I
will
say.
He
previously
founded
and
led
Emergence
Therapeutics.
I
worked
with
him
for
that
company
as
well
as
an
advisor.
And
this
is
an
ADC
company
that
was
acquired
by
El
Aleli
in
2023,
and
now
have
brought
together
a
seasoned
team,
created
a
seasoned
team,
including
me
as
an
advisor
at
Adcytherix
to
build
the
company
as
a
next
generation
ADC
design
platform,
as
well
as
ADC
development
company,
is
advancing
multiple
ADCs
in
high
and
medical
need
area.
Rakesh Dixit
And
since
its
launch,
I've
learned
to
say
that
with
Jack's
credit
at
Scythix
has
attracted
strong
international
investor
support,
including
over
$30
million
seed
finance,
30
million
euro
seed
financing
and
our
over
105
million
dollar
Series
A
funding
for
ADC
pipeline.
Jack
is
brings
a
rare
combination
of
scientific
vision,
company
building
experience,
and
deep
knowledge
of
ADC
backed
development.
Today
we're
going
to
discuss
the
evolution
of
ADC
field
and
what
is
needed
to
create
truly
differentiated
next
generation
ADCs
and
how
at
SiteSix
is
positioning
itself
to
developing
these
comp
this
highly
differentiated,
comparative,
highly
competitive
oncology
ADCs.
So,
Jack,
welcome
to
the
podcast.
Before
I
get
started,
do
you
want
to
say
a
few
words
about
you
or
before
I
get
into
questions?
From Neuropharmacology To Biotech CEO
Jack Elands
Yeah,
well,
first
of
all,
thanks,
Rakesh,
for
the
introduction.
Good
morning,
good
afternoon,
depending
on
where
you
are.
Good
afternoon
for
me.
I'm
based
in
Brussels.
Yeah,
I'm
I
was
trained
basically
as
a
neuropharmacologist.
So
it's
been
you
know
it's
been
a
long
road
to
end
up
in
in
oncology.
After
having
spent
a
number
of
years
doing
pure
academic
research,
I
made
a
jump
to
the
pharmaceutical
industry
at
Marion
Meraldao
in
Strasbourg,
now
better
known
as
SAFI.
And
that
center
basically
was
a
center
for
development
of
drugs
that
you
know
central
nervous
system-based
diseases.
After
a
while,
I
got
involved
in
the
automation
for
drug
screening,
developed
data
management
because
the
hand
systems
couldn't
cope
with
it
anymore.
And
because
of
all
that
work,
I
ended
up
in
redefining
with
the
team
the
lead
generation
and
discovery
effort,
and
that
made
me
view
a
larger,
a
much
larger
piece
of
the
business
than
ever
before
as
a
scientist.
And
from
that
moment
on
I
could
only
live
in
the
biotech
world
because
it
was
it
was
too
difficult
to
go
back
and
to
work
in
a
very
limited
segment
within
the
industry.
Jack Elands
So
I
effectively
joined
the
the
various
biotech
companies
and
ultimately
ended
up
launching
my
first
company.
This
was
in
2010
in
Belgium,
a
company
called
Amakem
Therapeutics,
where
we
developed,
this
was
probably
the
closest
to
my
neurology
background
or
neuropharmacology
background.
We
developed
drugs
to
treat
glaucoma,
so
intraocular
pressure.
We
developed
that
up
until
phase
two
and
then
sold
the
business
to
a
Korean
group.
And
then
from
there
on
in
2015,
I
basically
made
a
jump
to
antibodies
and
oncology.
I
took
on
the
helm
of
Blink
Biomedical,
an
amalgamation
of
Blink
therapeutics
out
of
cancer
research
technology
on
the
one
hand,
and
the
antibody
business
from
Valneva
on
the
other
end,
that
became
Blink
Biomedical.
From
Blink,
I'm
still
actually
involved
with
Blink
because
there
is
some
deals
that
create
long-term
revenues
that
I'm
still
administering,
but
it's
a
very
small
piece
of
my
activity.
At
some
point,
we
were
asked
by
Kirma
partners
in
Paris,
an
investor
in
Paris,
who
were
invested
also
in
Blink,
whether
I
was
interested
to
take
on
a
mandate
to
look
at
Nectin
4
as
a
potential
ADC
target.
At
that
time,
you
know,
CGIN
was
already
developing
Enfortima
Phototin,
later
better
known
as
PATSEF,
and
now
on
the
market,
of
course.
Jack Elands
And
after
taking
a
good
look
at
that,
we
thought,
yes,
it's
a
it's
possible
to
develop
a
best-in-class
based
on
the
proof
that
Enfortima
Phodotin
had
given
that
it
would
actually
it
actually
is
a
good
drug
to
treat
bladder
cancer.
So
we
we
had
a
collaboration
with
the
Center
of
Cancer
Research
in
Marseille,
together
also
with
the
local
cancer
hospital,
which
is
one
of
the
more
most
renowned
cancer
hospitals
in
France.
We
set
up
a
company
that
was
a
basically
having
a
French
German
company
with
a
holding
in
in
Germany,
but
with
the
active
the
biotech
development
area
in
in
Marseille,
in
France.
And
we
developed
a
DAR-8
exoticon-based
Nyctin
4
ADC
that
was
the
best
in
class
after
PATSEF.
We
never
made
it
to
the
clinic,
right
before
we
were
we
had
already
filed
a
CTA,
and
then
Lily
basically
knocked
on
the
door
and
acquired
us
before
we
were
able
to
to
go
into
the
clinic.
That
was
in
August
2023.
Unfortunately,
Lily
has
just
announced
that
this
drug
has
been
stopped.
Lily
was
developing
two
Nectin
4
ADCs
with
the
Exatcon
or
Exatcon-like
payloads,
and
they
have
stopped
ETX22,
even
though
I
know
from
having
spoken
to
principal
investigators
that
the
drug
actually
is
very,
very
efficacious
and
has
a
very
high
level
of
objective
response
rate.
Lilly
acquired
us
in
August
2023,
and
they
required
me
to
step
down.
I
didn't
feel
that
the
business
was
finished
and
that
there
were
still
lots
of
things
to
be
done
in
the
ADC
field.
So
I
got
together
with
Pontifax,
Ran
Nusbaum,
and
basically
asked
them
if
they
were
willing
to
help
me
to
set
up
another
company.
Rand
basically
told
me
that
he
was
about
to
ask
me
the
same
question.
We
then
spent
a
couple
of
months
to
work
out
the
business
model,
make
sure
that
the
people
that
I
wanted
to
bring
along
were
freed
from
any
any
emergence
or
Lily
background.
And
then
in
April
2024,
we
started
AtSetherix.
Building A New ADC Company Fast
Jack Elands
The
idea
of
Adcytherix
is
to
build
ADCs
with
payloads
that
can
overcome
resistance
that
is
created
by
treat
by
treating
patients
with
either
jubilin
or
topoisomerase
inhibitor
one-based
ADCs.
But
when
we
started
the
company,
we
had
basically
the
idea,
but
not
a
real
good
sense
of
how
to
go
about
it.
So
we
built
the
company
around
an
asset
that
is
not
unlike
ETX22
following
PATSEF.
So
here
we
don't
yet
disclose
the
target,
but
here
we're
basically
following
a
tubulant-based,
tubulant
inhibitor-based
ADC,
where
we
are
developing
a
best-in-class
targeting
a
target
that
is
now
better
known
than
when
we
started,
where
there
is
a
first-in-class
ADC
being
developed
in
late-stage
clinical
trials,
and
where
we
know
very
clearly
that
we
will
be
able
to
develop
a
best-in-class,
a
real
best-in-class.
We
started
with
a
30
million
euro
seed
round
that
was
led
by
Pontifax.
Jack Elands
We
brought
in
RA
Capital,
KKR
through
their
DORM
bio
platform,
and
WUSHI
made
an
investment
direct
and
via
Pureios.
And
then
in
October,
we
finalized
the
Series
A
of
105
million
euro,
where
BPI
France,
Kirma,
Andira
partners,
Angelini
Ventures,
and
Amoon,
as
well
as
Surveyor
from
Cadell
joined
us.
So
now
we're
well
funded.
We
as
I
mentioned,
we
started
with
the
DEAT
program
where
we're
developing
the
best
in
class.
We
do
that
based
on
a
DAR4
exat
econ
type
structure.
And
we
were
able
to
dose
the
first
patients
within
two
years
since
the
start.
And
so
we're
in
early
dose
escalation
at
the
moment.
We've
just
done
the
first
dose
level,
and
we
should
have
our
dose
escalation
meeting
mid
this
month.
So
it's
exciting
times.
But
as
I
mentioned,
the
key
thing
that
we
were
interested
in
for
at
Cytherix
is
really
looking
at
novel
payloads.
Why The Field Needs Novel Payloads
Jack Elands
And
one
of
the
first
payloads
that
we
looked
at
is
from
the
family
of
trabectadin
and
lurbinectadin,
compounds
developed
by
Pharmamar
and
on
the
market
to
treat
various
different
indications.
We
went
for
Lurbinectadin
for
a
variety
of
different
reasons,
and
lurbinectadin
is
basically
approved
to
treat
small
cell
lung
cancer
in
the
US,
and
it's
in
clinical
trials
for
a
number
of
other
indications.
The
mechanism
of
action
of
these
payloads
is
very
different
than
from
tubulin
or
topoisomerase
1
inhibitors,
and
that
makes
them
ideal
candidates
to
follow
on
to
treat
patients
that
have
developed
resistance
against
the
current
generation
of
ADCs.
People
that
with
knowledge
in
the
field,
it
will
not
have
gone
unnoticed
that
almost
every
ADC
that's
being
developed
today
is
equipped
with
the
topoisomerase
1
inhibitors.
The
first
ones
were,
of
course,
NHER2
and
the
rest
of
the
DIEC
stable
using
the
Rixtecon,
but
then
a
large
number
of
ADCs
were
developed
with
Exitcon
or
Exitcon
derivatives.
And
the
amount
of
ADCs
that
are
being
developed
in
this
field
with
topo
1-based
ADC
payloads,
it's
just
too
much.
Patients
will
have
will
develop
resistance.
So
it's
critically
important
that
we
follow
on
with
payloads
that
can
overcome
that
resistance.
Jack Elands
And
that's
what
the
rest
of
the
pipeline
of
the
company
is
about.
We've
just
put
into
development
the
first,
which
is
trestizomap
using
Lurbinictidin.
And
there
we're
basically,
amongst
others,
going
after
patients
that
have
been
treated
with
NHER2
and
that
have
developed
resistance.
I
think
if
you
look
at
the
latest
literature
in
this
area,
we
see
more
and
more
reports
that
patients
treated
with
NHER2
actually
do
develop
resistance.
And
that
oftentimes
this
resistance
is
related
to
changes
in
the
way
that
the
topoison
rase
one
inhibitors
can
work.
It
could
be
efflux
pump
upregulation,
it
could
be
changes
in
the
topo
isomerase
gene
point
mutation
so
that
these
inhibitors
don't
bind
so
well
anymore,
etc.
etc.
But
it's
sometimes
also
the
target.
There's
a
very
well-known
example
of
drop
point
mutation
that
takes
us
off
the
membrane.
And
internally
internally
in
the
cytoplasm,
you
see
accumulation.
But
the
majority
of
cases
of
inhibition
sorry
of
resistance
are
really
about
the
payload.
Career Turning Points And Value Creation
Rakesh Dixit
That's
fantastic.
and
and
thank
you,
Jack,
for
you
know,
you
know,
educating
us
with
your
journey
in
the
up
to
the
ADC
field
here.
You
have
a
long
career
in
RD.
So
the
first
question
that
I
have
for
you,
Jack,
that
what
actually
sparked
your
interest
in
science
and
led
to
the
biopharmaceutical
RD
over
your
30
years
or
more
longer
career
in
biopharma,
what
moments
most
shaped
your
path?
You
know,
like
moving
from
the
neuropharmacologist
to
the
antibody
to
the
ADCs?
You
know,
what
were
the
critical,
you
know,
you
know,
time
points,
you
know,
in
your
career
where
you
said,
okay,
this
interests
me
more
now
than
the
other
ones,
and
you
know,
that
guest
stuff.
Jack Elands
Yeah.
Good
question.
I
think
I
considered
myself
a
fundamental
academic
scientist.
anything
that
was
you
know,
like
drug
development,
that
wasn't
that
I
wouldn't
say
it
wasn't
science,
but
that
was
not
what
I
was
interested
in.
The
change
really
came
when
I
joined
Marion
Aldao.
I
was
I
was
asked
to
set
up
certain
activities
only
to
find
out
that
when
I
was
there,
I
was
basically
replacing
a
person.
So
we're
talking
about
the
early
90s.
That
was
still
money,
it
was
not
an
issue.
And
so
I
was
basically
replacing
a
person
who
had
left
and
that
nobody
wanted
to
work
with.
And
so
the
first
reaction
was
do
whatever
you
want,
just
don't
get
us
involved.
That
I
found
something
that
I
couldn't
understand.
So
I
started
wandering
around,
talking
to
people,
and
basically
found
out
that
the
chemists
were
complaining
that
you
know
the
molecules
that
they
made
didn't
get
tested.
So
I
said,
Well,
we
can
fix
that.
And
so
I
started
building
a
profiling
screening
platform
that
grew
to
a
center
that
all
the
four
research
sites
of
Mary
Melda
would
submit
as
samples
to,
and
we
built
a
lot
of
automation
around
that.
And
it
was
a
at
the
time,
it
was
such
a
logical
step
for
me
to
not
do
something
that
nobody
wanted,
and
yet
look
at
how
people
needed
things
and
where
I
could
be
useful.
It
was
almost
like
an
automatic
breaking
away
from
my
academic
mindset
and
becoming
very
in
industrial,
very
very
focused
on
adding
value.
Jack Elands
And
not,
I
think
it
wasn't
so
illogical
that
once
I
saw
the
broader
business
aspect
having
been
in
this
lead
generation
optimization
effort,
that
you
know,
I
became
more
attracted
to
the
whole
idea
from
starting
in
very
early
in
conceptually
you
know
developing
a
program
to
develop
a
drug,
and
then
also
you
know
looking
at
at
the
end,
the
financials,
the
marketing,
and
the
business
development,
etc.
That's
why
I
went
to
biotech.
But
again,
initially
my
biotech
efforts
were
very
focused
on
they
were
very
focused
on
um
on
small
molecules,
and
only
later
I
started
to
get
more
interested
in
in
antibodies.
I
think
my
my
the
change
from
Amachem
to
Blink
was
one
of
having
seen
the
power
of
biologics
and
looking
at
a
a
more
practical
way
to
develop
drugs
faster
than
with
small
molecules.
And
it
was
it
was
an
idea.
I
you
know,
I
can't
say
that
all
biologics
are
developed
faster,
but
it
there
are
I
think
there
are
certain
ways
to
to
skip
things
and
do
fast
do
things
faster
with
biologics
than
you
can
do
with
small
molecules.
And
um
with
Blink
we
went
a
long
way.
We
developed
the
CD47
asset
that
we
then
ultimately
sold
to
to
Gilead.
and
we
did
a
back
license
to
Genmap.
GenMap
has
for
a
long
time
been
developing
by
specifics
based
on
the
C
D47
asset,
but
I
unfortunately
never
was
able
to
get
this
into
the
clinic
myself,
or
myself,
but
at
least
directly,
in
contrast
to
the
glaucoma
program
that
we
you
know
we
developed
up
until
phase
two.
And
so
the
idea
to
leave
the
because
C47
is
essentially
in
you
know
it's
an
immuno
oncology,
and
immuno
oncology
is
it's
not
an
easy
field.
It's
a
very
delicate
field
with
lots
of
intricacies
on
how
proteins
are
being
regulated,
the
immune
system
is
is
almost
immune
for
changes
and
manipulation.
Jack Elands
So
the
idea
of
developing
or
looking
for
an
ADC
where
you
use
the
antibody
basically
only
as
an
address
to
find
the
cancer
target
and
then
deliver
the
bomb
to
kill
it,
I
thought
was
very
attractive.
And
it
really
was
something
that
I
wanted
to
put
my
weight
behind.
We
spent
a
lot
of
time,
I'm
talking
about
Xavier
Preville
and
myself
to
build
a
business
clause.
This
is
actually
where
you
and
I
first
met,
and
where
we
laid
out
a
development
plan
up
until
the
moment
that
we
could
execute
it
and
then
started
the
company.
So
it's
a
gradual
process
of
having
been
very
opportunistic
at
Marion
Meraldow,
not
wanting
to
do
something
that
wasn't
useful
in
the
context
of
a
pharma
company
and
looking
for
the
best
way
to
make
myself
useful.
That
was
probably
the
biggest
change
in
my
career
that
I
can
think
of.
The
others
were
smaller
changes,
even
though
you
know
they
got
me
where
I
where
I
am
right
now
and
they
were
important.
Let
me
add
one
thing
that
I
often
talk
about
with
new
CEOs
or
soon-to-be
CEOs.
I
actually
have
spent
some
years
in
in
strategic
marketing
and
business
development,
the
commercial
business
development,
so
selling
stuff.
It's
an
incredibly
valid
experience
to
do
that.
I
think
most
of
us
that
are
in
the
biotech
world,
we
don't
have
the
a
good
sense
of
what
we're
doing
when
we're
raising
money,
when
we're
talking
to
investors.
And
the
commercial
business
development
background
for
me
has
been
an
absolutely
great
teacher
on
you
know
how
best
to
look
at
that,
how
to
control
that
process.
That
is
something
that
came
over
time.
It's
not
been
one
moment,
but
if
anything
has
shaped
my
career,
it's
also
that.
That
the
commercial
business
development
background
has
really
been
very,
very,
I
wouldn't
even
say
helpful,
but
critical
in
getting
me
where
I
am
today.
Patient Impact As The North Star
Rakesh Dixit
Yeah,
this
is
a
fantastic,
great
advice,
Jack.
And
I'd
100%
agree
with
you.
And
and
looking
at
this,
you
know,
given
that
you
have
worked
with
lots
of
different
programs,
lots
of
different
things
you
have
done
in
your
career,
even
in
the
areas
where
nobody
wanted
to
go,
you
went
there,
you
know,
took
some
risk
in
your,
you
know,
in
your
career.
Of
all
the
programs
that
you
have
worked,
you
know,
in
your
career,
which
project
or
experience
you
felt
that's
most
rewarding,
has
been
most
rewarding
scientifically,
professionally,
or
personally?
Not
necessarily
on
the
money
side.
I'm
just
talking
about
more
from
it,
something
that
you
said,
you
know
what,
I
feel
good
about
this,
you
know.
And
both
scientifically
and
professionally
and
personally.
Jack Elands
Yeah,
yeah.
No,
it's
a
very
valid
question.
And
you
know,
I
can't
ignore
the
fact
that
it's
good
to
develop
a
drug
to
treat
patients
that
have
glaucoma.
But
nonetheless,
there
are
drugs
that
can
treat
glaucoma.
So
there's
there's
opportunities
there,
you
can
do
it
better.
But
in
oncology,
I
think
it's
different.
You're
not
okay,
you
can
do
things
better,
but
ultimately
you're
you're
helping
patients
to
live
longer
and
ideally
under
reasonable
quality
of
life
conditions.
Correct.
And
I
think
for
me,
it's
the
major
reason
that
after
emergence
I
wanted
to
continue.
It's
just
the
focus
on
being
able
to
help
patients
that
is
really
very
important.
And
I
also
tell
this
to
the
team,
to
the
people
in
the
company,
I
tell
it
to
my
investors,
I
tell
it
to
other
investors,
that
our
focus
is
really
not
to
bring
value
for
investors,
but
to
bring
bring
value
for
patients.
And
if
we
bring
value
for
patients,
all
the
rest
will
fall
in
line
automatically.
And
it's
that
idea
that
you
know
patients
who
I'm
I'm
talking
now
about
outside
virus,
but
it's
in
general.
But
if
you
think
about
a
patient
who's
being
treated
for
breast
cancer
and
then
and
her
term
no
longer
works,
these
women
have
no
option
left.
So
it's
exciting
and
and
and
and
really
reinvigorating
for
a
person
like
myself
to
be
able
to
work
on
this
and
to
develop
drugs.
So
the
more
I
get
along,
actually,
the
more
I
find
it
satisfactory
because
the
more
you
learn,
the
better
you
can
hone
in
on
the
diseases
where
patients
need
new
drugs
most.
And
of
course,
in
oncology
remains
a
field
after
all,
whereby
it's
basically
a
question
of
life
and
death.
And
in
many
cases.
So
if
you
can
have
if
you
can
make
a
difference
there,
yeah,
it's
it
really
is
personally
is
very
it's
it's
very
important
to
me.
Rakesh Dixit
No,
I
fully
agree
with
you
because
I
think
the
question
of
resistance
is
is
coming
up
a
lot
nowadays,
despite
the
fact
there
will
be
people
saying,
Well,
why
do
you
want
to
develop
another
Hart
to
ADC?
You
know,
what's
what's
the
point
when
there
are
you
know
maybe
30,
40
LED
ADCs,
you
know,
targeting
HAD2.
But
your
concept
or
your
strategy
of
developing
an
ADC
for
resistant
patients,
you
know,
patients
who
are
not
responding
to
current
HA2
therapies
is
is
really
great.
Announcement
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you
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conversation?
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If
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or
topic
ideas,
we'd
love
to
hear
those
too.
You
can
send
them
in
a
podcast
review.
Ethics, Toxicity, And Quality Of Life
Rakesh Dixit
And
since
I'm
a
toxicologist,
as
you
know,
I
will
have
to
have
that
question,
this
question,
the
next
one.
So,
to
me,
how
do
you
balance
the
excitement
of
breakthrough
science,
breakthrough
ADCs,
with
the
ethical
duty
that
we
all
have
to
protect
patients
from
the
harm?
You
know,
what
what
we
need
to
do
either
preclinically
and
clinically
to
make
sure
that
we
are
not
harming
undue
patients,
patients
unduly
without
without
giving
them
something
in
return.
You
know,
I
mean
With
the
cancer
therapy,
we
all
know
there
will
be
toxicities.
But
at
the
same
time,
we
want
to
give
them
more
benefit
than
the
than
the
than
these
than
the
toxicity,
because
these
toxicities
also
affect
the
quality
of
life
for
patients,
you
know.
Because
there
is
no
there's
no
point
in
saying,
okay,
you
have
two
months
extra
or
five
months
extra
to
live
with
on
my
drug,
but
your
life
will
be
miserable
with
all
the
toxicities.
You
know,
a
good
example
is
PATSA,
where
patients
suffer
a
lot
from
peripheral
neuropathy
and
you
know,
newtopenias,
infection
rates,
and
all
this
stuff.
Skin,
not
to
mention
skin
toxicities.
And
I
think
what
I
liked
when
I
was
working
with
you
on
the
nectin-4
program,
you
did
something
to
prevent
that,
you
know,
by
developing
a
more
differentiated
nectin
4
ADC.
So
I
would,
yeah,
so
more
elaborate
on
a
little
bit
more
on
Reducing Skin Toxicity In Nectin-4
Rakesh Dixit
that
one.
Yeah.
Jack Elands
Yeah.
So
let
me
start
on
Nectin
4
and
then
move
on
to
what
we're
doing
today.
So
yeah,
nect
if
you
look
at
PATSEF,
it
was
obvious
from
talking
to
the
clinicians
that
's
it
causes
peripheral
neuropathy.
But
it
the
most
important
thing
of
PATSEF,
which
is
a
negative
differentiator,
is
skin
tox.
And
but
by
when
talking
to
the
clinicians,
and
in
particular
to
Jonathan
Rosenberg
and
Sloan
Kettering,
he
said,
Jack
said
the
skin
tox
may
not
be
that
bad,
but
it
makes
patients
decide
to
stop
being
treated.
And
so
that's
bad.
And
that
needs
to
be
fixed.
So
what
we
did
is
we
at
the
time
we
didn't
know
how,
but
we
felt
it
was
important
that
we
develop
an
AD
an
antibody
that
would
bind
to
nectin
4
on
the
cancer,
but
not
on
the
carotenocytes
in
the
skin.
We
didn't
know
how
to
do
it.
So
we
basically
put
together
a
functional
screen
whereby
we
screened
the
antibodies
both
in
the
cancer,
in
the
model
of
course,
and
then
on
freshly
isolated
carotenocyte
from
human
skin.
And
we
found
antibodies
that
did
the
job.
It
goes
maybe
a
bit
far
to
go
through
the
scientific
explanation,
but
you
know,
we
have
two
basic
theories
of
of
why
this
may
work
these
days.
And
then
we
went
through
the
testing
of
what
became
ETX22
using
that
specific
antibody,
and
we've
never
found
an
instance
of
skin
tox.
I
threw
the
grave
pan,
you
know,
because
we
have
no
formal
official
communication,
it
appears
that
ETX22
has
never
caused
skin
tox.
And
that,
of
course,
is
is
very
important.
Jack Elands
So
I
think
there
with
the
Nectin
4
ADC,
we
did
our
best
to
avoid
skin
tox,
and
it
seems
that
we've
been
successful.
When
we
started
at
Cytherix
looking
for
novel
payloads,
I
basically
defined
a
number
of
rules
of
thumb
to
select
novel
payloads.
One
was
they
shouldn't
be
too
potent
because
we
know
that
the
over
the
ultra-potent
payloads,
they
don't
they're
not
manageable.
The
other
is
that
it
shouldn't,
you
know,
it
should
also
be
potent
enough.
I
don't
want
something
that
is
a
lot
less
potent
than
the
Ruxticon.
But
I
think
the
most
important
rule
that
we
put
together
is
let's
find
the
payloads
from
drugs
that
are
already
approved
as
anti-cancer
drugs.
And
if
you
pick
those,
you
actually
do,
and
lurbinectin
is
one,
it's
being
used
for
the
treatment
of
small
cellular
cancer
in
the
US.
You
have
a
payload
with
be
it
a
small,
but
with
a
payload
with
a
therapeutic
index.
The
other
payloads
that
we're
using
today,
they
cannot
be
used
as
a
standalone
drug
in
men.
They're
too
toxic,
so
they
have
a
negative
therapeutic
index.
Now
we
have
a
payload
with
a
therapeutic
index
that's
positive,
even
if
it's
small.
So
I
think
we
know
that
there
is
a
dose
that's
I'm
not
gonna
say
that
it's
you
know
nice,
there
are
toxicities,
but
it's
a
tolerable
dose.
And
so
we
should
be
able
to
get
to
an
ADC
with
a
dosing
regimen
where
the
toxicities
are
lower
than
with
the
most
of
the
toxins
that
we
use
these
days.
It's
it's
the
goal,
it's
part
of
what
we
want
to
do,
and
and
we're
putting
it
in
place
as
we
speak.
Lurineicin
is
a
good
example
of
that.
We
have
other
payloads
that
are
slightly
less
advanced
and
that
I
can't
disclose
now,
but
there's
one
payload
in
particular
that
doesn't
cause
cytopenias.
Jack Elands
Now,
if
this
payload
would
work
and
we
would
not
have
any
neutropenia,
you
know,
that
means
that
patients,
when
they're
treated
and
they
they
there's
no
risk
of
root
neutropenia,
they
can
just
go
home.
They
don't
have
to
stay
hospital
to
combat
infections.
So
these
are
these
are
things
where
I
think
we
can
really
look
at,
on
the
one
hand,
the
benefit
of
an
ADC,
you
know,
with
a
very
much
more
targeted
therapeutic
treatment
rather
than
the
earlier
generations
of
cancer
therapies,
but
then
also
you
know,
combining
it
with
compounds
that
are
that
are
known
to
work,
first
of
all,
against
cancer
and
that
have
a
therapeutic
index,
and
hopefully,
ideally
get
an
ADC
that
is
more
tolerable
and
that
therefore
can
be
dosed
longer,
and
that
can
therefore
help
patients
for
a
longer
time.
Because
as
you,
as
much
as
you
know,
patients
do
not
always
stop
an
ADC
treatment
because
of
progression
of
the
tumor.
They
may
just
be
fed
up
with
GI
tox
after
having
been
treated
with
a
topo
1-based
ADC.
They
may
be
fed
up,
like
in
the
case
of
a
PATSEF
with
skin
tox.
The
toxicities
that
ADCs
cause
often
are
a
reason
for
patients
to
discontinue
treatment.
And
that
is,
of
course,
a
problem
that
needs
to
be
fixed.
Rakesh Dixit
No,
I
think
that's
very
well
said,
Jack.
And
I
just
came
back,
you
know,
a
couple
of
weeks
back
from
the
ACR
meeting,
and
there
has
been
a
lot
of
discussion
in
the
ADC
field
on
the
novel
payloads.
And
just
not
a
novel
payload
for
the
sake
of
it.
It's
the
novel
payloads
that
can
maintain
reason,
you
know,
pretty
good
efficacy
in
patients,
but
but
not
increasing
toxicity,
in
fact,
decreasing
some
of
the
adverse
effects
that
are
not
well
tolerated
by
patients,
because
you
know,
this
just
not
a
toxicity,
it
also
affects
the
quality
of
life
of
patients.
And
as
you
said,
that
that
quite
often
is
the
major
reason
why
patients
don't
want
to,
you
know,
take
anymore
that
drug.
I
mean,
if
I
had
cancer
and
if
I
cannot
get
up
in
the
morning
and
you
know,
close
my
buttons,
you
know,
or
continuously
seeing,
you
know,
on
the
antibiotics
for
the
infections
or
something
else,
I
think
I
will
consider
switching
it
to
some
different
therapy.
And
I
think
to
me,
the
quality
of
life
is
directly
linked
with
the
with
the
toxicity
of
ADCs,
as
well
as,
of
course,
the
cancer
itself
has
got
its
own
toxicity
problems,
you
know,
because
of
the
you
know,
cancer
effects
not
only
it
affects
a
lot
of
physiological
functions
in
the
body,
and
that
can
also
impact,
like
especially
getting,
you
know,
being
tired
all
the
time
and
all
this
stuff.
But
but
definitely
on
the
safety
side,
I
really
like
that
approach.
Choosing Safer Payloads With Therapeutic Index
Rakesh Dixit
So
coming
back
to
the
future
of
ADCs,
okay,
because
that's
what
I
want
to
focus
today
in
this
this
podcast.
That
in
your
experience
or
in
your
thinking,
what
do
you
think
is
the
which
therapeutic
ADC
modality
the
thing
will
define
in
next
decade
and
why?
Because
I
came
back
from
a
from
the
ACR
meeting
and
I
saw
a
very
crowded
ADC
field.
And
actually
I
wrote
something
in
the
in
the
LinkedIn
that
it's
not
the
it's
not
the
ADC
field
is
crowded,
it's
crowded
with
very
undifferentiated
ADCs.
You
know,
what
which
I
meant
by
me
too,
okay.
This
person
has
it,
so
I
need
to
have
this,
you
know,
that
this
company
has
it,
so
I
need
to
have
it.
Like
a
good
example
is
like,
you
know,
you
know,
Hart2
space,
BCMA
space,
you
know,
B7S3.
And
I
looked
at
a
lot
of
these
posters
and
said,
you
know
what,
what's
new?
Okay,
what
exactly
new
you
are
doing?
You
know,
did
you
did
you
invent
a
new
payload
or
or
or
somehow
you
think
this
will
change
the
the
the
differentiated
enough?
And
and
I
did
not
see
that.
So
what
I'd
like
to
hear
from
your
point
of
view,
what
do
you
think
the
next
decade
in
the
ADC
field
will
come?
Because
a
lot
of
people
ask
me,
you
know,
that
similar
to
the
checkpoint
inhibitor
therapies,
PD1,
PDL1
based,
you
know,
things
went
at
the
peak,
and
now
nobody
wants
to
invest
much
money
in
those
therapies
because
they
just
don't
see
differentiation.
You
know,
they
say,
how
many,
how
many
PD1s
we
can
develop,
how
many
PDL1s
we
can
develop?
And
same
thing
we
are
seeing
in
biospecifics
as
well,
where
you
know,
almost
every
single
week
I
see
somebody
developing
another
BC,
BCMA,
CD3,
you
know,
engage,
T
cell
engage,
TCEs,
you
know.
I
mean,
how
many
it
is
it
really
helping
patients
or
are
you
just
making
a
Me
Too
drug?
So
the
question
is
what
do
you
expect?
What
will
happen
to
ADC
field
in
let's
see
next
10
years?
Where
you
think
we'll
be
going?
So
just
about
to
hear
your
thoughts,
A Framework For Sequencing ADCs
Rakesh Dixit
you
know.
Yeah.
Jack Elands
Yeah,
I
think
in
general,
Rakesh,
but
let's
take
you
know,
PD1,
PDL1
for
an
example.
The
the
development
cost
is
so
high
that
it
is
actually
useful
that
a
number
of
companies
work
on
PD1,
PDL1s
and
then
have
you
know
various
different
clinical
trials.
Because
I
don't
think
there
would
be
as
much
power
and
push
for
extending
the
boundaries
of
the
potential
treatment
if
it
was
done
by
only
one
company.
But
there
is,
of
course,
a
cap
on
it.
At
some
point
it
becomes
counterproductive,
and
you
could
actually
ask
that
it's
no
longer
ethical
either
to
invest
so
much
money
in
you
know
in
number
10
and
number
15.
And
we
see
that
effectively
with
ADCs.
There
are
too
many
Topo
1-based
ADCs,
you
know,
and
the
targets
are
not
that
innovative
that
the
the
it
is
warranted
that
so
many
topo
one-based
ADCs
are
being
developed.
So
for
the
moment,
we're
not
able
to
cure
cancer.
At
least
there
are
a
number
of
cancers
that
we
can
reasonably
cure,
but
the
vast
majority
of
solid
cancers
we
can't
cure.
So
I
think
the
goal
for
us
as
a
drug
development
community
in
oncology
is
to
extend
patient
lives
in
the
best
possible
way,
making,
you
know,
maybe
not
curing
the
cancer,
but
being
able
to
live
with
the
cancer,
kind
of
live
in
peace.
A
little
bit
like
what
happened
with
the
AIDS
therapies
over
time,
where
you
know,
people
that
are
positive,
HIV
positive,
still
can
lead
a
normal
life
if
they
if
they
follow
the
appropriate
medication
these
days.
That
might
be
a
possibility
where
that's
at
least
that
that
that
would
be
my
dream,
so
to
speak,
to
get
that
to
patients.
Jack Elands
And
I
don't
think
this
will
be
with
one
generation
of
ADCs.
It
will
it
will
it
will
require
a
series
of
various
ADCs
whereby
the
cancer,
when
it's
being
treated,
will
develop
some
form
of
resistance,
and
then
you
will
have
to
come
in
with
another
ADC
to
be
able
to
continue
to
treat
that
patient,
and
then
you
may
want
to
come
in
with
a
third
one,
etc.
And
so
we
actually
coined
the
term
a
cancer
treatment
framework
to
establish
this,
because
if
you
if
you
know
your
cancer,
or
if
the
the
if
the
doctor
knows
the
cancer
of
his
patient
or
her
patient,
then
you
could
actually
develop
a
treatment
algorithm
in
which
you
sequence
those
ADCs
and
maybe
not
even
wait
until
resistance
is
so
bad
that
you
you
have
to
but
but
start
to
treat
a
patient
with
another
ADC
that
basically
comes
in
afterwards.
So
that
idea
of
a
cancer
treatment
framework
is
something
that
we
we
formulated
a
while
back
to
see
if
we
could
develop
our
ADCs
accordingly.
So
the
first
step
could
be
right,
now
we
have
a
topo
one-based
ADC
like
NHER2,
patient
develop
resistance,
then
we
come
in
with
trustees
map
lurbinectadin.
Then
thereafter,
you
know,
there
is
a
possibility
to
come
in
with
yet
another
ADC
with
a
payload
that
is
clearly
differentiated
from
both
NHERT2
and
Lurbinectadin.
And
these
payloads,
these
drugs
exist,
so
we
can
pick
them.
Ultimately,
I
hope
that
the
combination
of
the
targeted
delivery
of
an
ADC
together
with
an
immuno
oncology
approach,
in
which
the
body
is
being
taught
to
kill
the
cancer
or
being
being
reinstructed
to
kill
the
cancer
would
would
work.
This
was,
of
course,
the
big
dream
after
PD1
PDL1
was
discovered.
Jack Elands
But
unfortunately,
most
of
the
other
immune
checkpoint
inhibitor
complexes
didn't
work
out
all
that
well.
And
so
there
is
a
long
way
to
go.
But
this
is
obviously
if
we
talk
about
curing
cancer,
that
obviously
is
the
ideal,
the
goal
that
we
all
should
strive
for.
And
maybe
that's
also
possible
with
an
ADC
by
by
only
locally
affecting
the
the
immunology
of
the
of
the
cancer
and
not
affecting
the
immunology
in
the
entire
body.
If
we
can
achieve
that,
that
would
be
great.
There
are
a
number
of
companies
that
have,
you
know,
that
are
brave
enough
to
go
after
this.
We
don't
have
that
scientific
knowledge.
We
don't
have
the
the
we
don't
have
the
connection
ourselves
with
a
groundbreaking
academic
lab
where
I
think
you
know
the
the
the
the
basic
idea,
the
basic
the
basic
science
teaching
you
that
something
may
be
possible
if
you
can
deliver
it
very
specifically
into
the
cancer.
That
combination,
if
we
can,
if
the
the
field
can
advance
the
ADC
technology
so
that
another
company,
another
academic
lab-based
company,
could
then
combine
that
with
an
immunocology
approach,
whether
it's
an
immunogonist
or
immuno
inhibitor,
depends
on
where
you
want
to
interact.
That
might
be
the
ultimate
goal,
you
know,
to
really
get
rid
of
cancer.
But
I
think
in
the
in
the
short
term,
I'm
still
thinking,
you
know,
in
tens,
at
least
10,
if
not
more
years,
getting
to
a
status
whereby
during
a
prolonged
period
of
time
a
patient
can
have
a
reasonable
certainty
that
he
can
live
in
peace
with
his
cancer
thanks
to
treatment
with
acceptable
side
effects.
Rakesh Dixit
Yeah,
some
maybe
give
him
more
cancer
as
a
chronic
disease.
Yeah.
Jack Elands
Yeah,
yeah.
That
would
be
that
I
think
that
would
be
a
great
first
step
towards
making
cancer
a
livable
disease.
Rakesh Dixit
So
on
the
same
topic
as
you
were
discussing,
on
the
combining
the
immunosy
therapy
that
have
really
helped
a
lot
of
patients,
and
then
obviously
now
on
a
little
bit
more
newer
therapies
like
ADCs
in
this
period
in
cancer.
Combination
of
these
two,
definitely
we
are
seeing
some
really
great
results,
especially
with
PATSIV
and
promulgum
web
combinations
and
some
others.
What
are
your
thoughts
on
developing,
like
targeting
two
targets
on
cancer
like
biospecifics
ADCs
with
a
novel
payload?
Or,
you
know,
having
the
same
target
or
biospecific
target
with
two
payloads
of
two
different
MOAs.
Not
necessarily
the
same
MOA.
I
don't
like
to
put
two
cyotoxic
payloads.
And
will
that
be
something
you
think
is
coming
in
the
future?
Because
I
saw
there's
a
lot
of
momentum
at
the
ACR
meeting
I
saw
where
I
got
my
hopes
up
that
there
is
opportunity
now.
People
are
looking
into
dual
payloads
with
different
MOAs
as
well
as
dual
targets
that
may
allow
to
bring
more
of
these
payloads
into
tumors
to
kill
them.
You
know,
what
are
your
thoughts
on
bi-specific
and
dual
payloads?
Bispecific And Dual Payload Reality Check
Jack Elands
You
know,
yeah.
I
think
they're
both
exciting.
We
don't
do
either
of
them,
but
that's
purely
for
a
reason
of
focus.
You
know,
we're
a
small
biotech,
we
need
to
have
focus
and
our
focus
is
on
on
novel
payloads.
That
doesn't
mean
anything
for
the
value
of
bi-specifics
or
dual
payload
approaches.
I
think
bi-specifics
can
be
really
interesting
in
in
further
enhancing
the
selectivity
for
cancer
only
and
and
and
avoiding
targeting
healthy
tissues.
There
is
still
work
to
be
done
there.
We
still
we
we
we
we
we
can
improve
on
that.
There
are
of
course
also
some
key
questions.
You
know,
if
you
have
a
bi-specific,
will
the
relative
affinities
for
both
both
targets
be
in
the
right
setting?
Which
target
do
you
want
to
engage
first
with?
Which
should
be
the
other
one?
It's
it's
a
delicate
all
of
a
sudden
you're
entering
into
a
field
where
there
are
many
more
questions
that
you
have
to
investigate.
You
know,
do
all
cancers
that
you're
looking
at
express
both
targets
in
in
the
right
ratio?
Is
there
heterogeneity?
Can
cancers
differentiate
in
terms
of
expression
levels?
Those
need
those
issues
need
to
be
understood,
and
they
will
probably
only
be
understood
once
these
bi-specific
ADCs
are
coming
to
the
clinic
and
see
how
patients
and
tumors
react
to
that.
But
in
itself,
I
think
it's
a
good
approach
to
make
more
selective
ADCs.
The
dual
payloads,
I
think
conceptually,
it's
beautiful.
Jack Elands
Unfortunately,
there's
a
pragmatic
piece
to
it.
You
know,
CMC,
the
behavior
of
those
molecules.
We're
just
touching,
we're
just
scratching
the
surface
of
those
dual
payload
ADCs.
Frankly,
when
I
mentioned
this
to
my
CMC
guy,
he
gets
an
instantaneous
headache.
It
it
you
make
your
you
make
your
life
very
much
more
difficult
um
if
you
do
that.
It
doesn't
mean
that
it
cannot
be
solved.
My
my
basic
warning
is
there
are
other
areas
that
also
need
attention.
Let's
avoid
on
just
going
after
this
because
we
can.
But
that's
you
know,
that's
easy
said.
Work
has
to
be
done,
people
have
to
sort
this
out.
And
I
think
right
now
people
are
also
doing
it
because
they
can.
And
I'm
I'm
I
agree
with
you.
Just
combining
two
cytotoxic
payloads
because
you
can,
that
doesn't
make
much
sense.
I've
seen
lots
of
examples
where
people
add
topo
one
and
tubulin-based
inhibitors.
You
will
come
to
the
clinic
and
you
will
be
behind
other
ADCs.
So
your
patient
will
have
probably
developed
resistance
against
top
of
one
inhibitors,
and
you
end
up
basically
with
a
tubulin
inhibitor-based
ADC.
So
I
think
people
have
to
be
smart.
If
you
do
something,
do
it
because
you
can
help
a
patient
live
longer
rather
than
because
you
can
you
know
technically
put
it
together.
Rakesh Dixit
Well,
I
think
that's
that's
what
I've
seen.
The
problem,
yeah,
yeah.
And
then
I
think
very
well
said,
and
I
think
that's
where
I
see
the
problem
with
lots
of
presentation.
I
saw
that
at
the
at
the
ACR
meeting,
that
the
thinking
process
is
what
you
know
people
are
trying
to
do
is
to
say,
oh,
because
I
have
these
two
payloads
and
I
can
combine
them,
but
without
thinking
about,
okay,
so
you
if
you're
going
to
combine
it
to
poison
with
inhibitors
like
exotal
or
DXT-like
molecule,
which
by
itself
causes
significant
neutropenia.
And
then
you
put
another
payload
MME
that
also
causes
neutropenia,
and
not
to
mention
other
toxicity
like
peripheral
neuropathy
and
all
that,
what
are
you
thinking?
You
know,
are
you
are
you
going
to
see
less
of
it?
And
and
if
if
you
think
less
of
it,
why?
You
know,
what
are
your
logic
on
that?
And
then,
you
know,
with
are
you
going
to
see
only
incremental
benefit
in
efficacy
or
more
toxicity?
What
the
therapeutic
index
looks
like.
When
you
when
you
talk
to
the
companies
who
are
doing
these
dual
payload
technologies,
I
have
seen
the
lots
of
companies,
they
don't
have
any
answer.
They
are
doing
it
just
because
they
can
do
it,
okay?
Or
they
have
they
have
somebody
convince
them
in
their
company
that
dual
payloads
will
make
a
lot
of
sense,
which
we
all
agree
with
with
that.
But
there
are
lots
of,
you
know,
to
me
personally,
in
selecting
dual
payloads,
you
got
to
do
a
lot
of
thinking,
you
know,
why
are
you
combining
with
what?
And
then
how
are
you
going
to
deal
with
not
only
the
issues
of
therapeutic
index,
but
also
the
CMC
problem,
as
you
mentioned?
How
are
you
going
to
scale
up?
All
that
is
stuck
is
still
in
is
not
well
thought
through,
at
least
in
my
experience.
Jack Elands
So
yeah,
I
would
agree.
I
would
agree.
And
then,
you
know,
I
think
if
you
more
than
one
clinician
has
told
me,
oncologist
has
told
me
that,
hey
Jack,
why
don't
you
just
develop
an
ADC
with
an
interesting
novel
payload
and
then
let
me
play
around
with
small
molecule
drugs
to
test
out
combinations
in
patients
that
that
make
sense?
Because
if
you
have
an
ADC
and
you
can
synergize
with
a
small
molecule
treatment,
maybe
that
small
molecule
is
not
as
toxic
as
it
is
when
used
as
a
standalone
molecule.
And
I
think
that
makes
a
lot
of
sense.
We
need
to
another
an
experiment,
it's
a
very
expensive
experiment
to
make
a
dual
payload
ADC.
And
I
think
we
need
to
very
carefully
investigate
whether
that
that
actually
makes
sense.
And
one
of
the
ways
to
do
it
is
to
combine
it,
you
know,
to
look
at
small
molecule
treatments
and
combine
it
that
way.
And
if
you
then
have
a
good
combination,
yes,
you
then
you
may
want
to
go
forward
and
develop
that.
Oh,
absolutely.
Rakesh Dixit
Like
combine
herbonectidin
is
small
cell
lung
cancer
with
an
ADC
that
that
also
targeting
the
you
know
the
the
lung
small
cell
lung
cancer.
Can
you
enhance
the
benefit
without
increasing
toxicity?
I
think
to
me,
and
if
that
does,
then
then
it
will
make
a
sense
to
make
a
dual
payload.
But
my
last
question
is
actually
it's
a
question
for,
of
course,
you
answered
some
of
it,
like
what
the
first-time
CEO
should
be
doing,
you
know,
and
I
you
you
said
that
having
that
having
that
background
or
experience
in
marketing
and
and
and
business
development
could
be
extremely
helpful.
So
so
I
think
those
are
those
are
the
great
points
you
already
described
that.
Defining A Lasting Contribution
Rakesh Dixit
So
just
a
last
question,
and
it's
a
more
hypothetical,
I
have
to
ask
you.
So
when
you
when
you
look
back
so
far
in
your
career,
and
people
say,
okay,
Jackie
Lance,
okay,
what
do
you
think
will
be
your
lasting
contribution
to
the
field
of
the
ADC
or
ADC
or
any
any
therapeutic
area
that
you
have
worked
on?
But
people
say,
Wow,
Jack,
you
know,
this
is
this
is
fantastic,
what
you
did,
you
know.
Jack Elands
To
be
very
honest,
at
the
moment
with
at
Cytherix,
I've
put
a
good
team
together
that
is
able
to
take
care
of
most
things.
And
what
I'm
trying
to
do
now
with
a
team
of
people
that
is
in
the
company
is
to
help
them
to
advance
their
careers
so
that
they
can
actually
become
successful
in
biotech
after
me,
so
to
speak.
So
I'm
I've
I've
never
done
this
so
much
as
as
I've
done
before.
I
enjoy
it
tremendously.
We
are
well
financed
so
that
I
can,
you
know,
I've
been
able
to
put
together
the
team,
and
it's
it's
it's
a
it's
an
immense
pleasure
to
help
other
people
develop
themselves
so
that
they
can
take
on
the
helm
because
there
is
there's
only
so
much
that
I
can
do.
This
is
probably
gonna
be
my
last
company
that
I'm
that
I've
set
up.
I
won't
stop
being
involved,
but
the
ability
to
help
other
people
to
advance
their
careers
and
to
guide
them
to
do
the
right
things,
that
is
something
that
that
I'm
enjoying
right
now,
and
it's
an
additional
goal
for
me.
You
know,
for
for
the
new
company,
it's
an
additional
goal
that
yeah,
we
we
we
prepare
a
next
generation
of
scientists
to
continue
the
biotech
Final Thanks And Sign-Off
Jack Elands
world.
Rakesh Dixit
No,
I
really
like
that
what
you
said,
and
and
and
you
know,
having
worked
with
you
since
2019
in
in
a
in
a
different
capacity,
like
a
more
advisor
consultant,
I
have
tremendously
enjoyed
working
with
you
and
learned
a
lot
from
you.
So
thank
you
for
this
podcast
and
your
guidance
and
your
enthusiasm
for
the
ADC
field,
and
really
appreciate
your
time
for
this
podcast.
And
and
thank
you
so
much.
Jack Elands
Thanks
a
lot,
Rakesh.
It
was
a
pleasure,
as
always.