NorthWest Biotherapeutics Inc (NWBO)

[ae kusterer]

MULHOLLAND: Control F in this 5/10/22 transcript, of the NYAS day of infamy , brings up no " cure" word .Why is Mulholland using the " cure " word on 4/10/23 in a Times interview ?

https://www.youtube.com/watch?v=Gshv4VWU9JQ

https://twitter.com/alphavestcap/status/1646576625536958471

“The average survival for glioblastoma is nine months,” he says. It is perhaps surprising, then, to hear Mulholland insist: “I’m actually very optimistic that we will cure it, and it could be very soon.”

https://www.thetimes.co.uk/article/60dd1a6c-d77e-11ed-80bc-e358583c5d62?shareToken=dbe49839a1865fcfb2643ccb910b8904

said your next session's about to start during sessions
0:35
welcome back everybody i hope you enjoyed the break
0:41
it would be great if we could get started with the next session
0:51
it's my pleasure to return the podium back to dr george the boyco who would announce the next presentation
1:12
okay some people are still filtering in um but it is my distinct pleasure to
1:18
introduce the next uh speaker uh it's another virtual presentation um holland
1:25
from the university college london hospitals a medical oncologist he treats brain
1:31
cancers exclusively he's chair of the cancer care and cns tumor board there
1:38
so paul i see uh you're there um and the title of his talk is uh
1:45
autologous tumor lysate loaded dendritic cell vaccination for glioblastoma well
1:50
thank you um i'd like to say um thank you very much
1:56
to the organizing committee and also to linda liao for asking me to do this
2:02
presentation linda was due to do the presentation today but unfortunately she's unwell but i can tell you it's my
2:09
absolute privilege to share this data with you i hope you find it as exciting as i
2:16
think it is so um i'm gonna today be presenting the
Glioblastoma
2:25
final results from the dc max l phase three trial
2:31
um and um and discuss with you the innovative trial design and also share
2:39
the results um what do we know about glioblastoma
2:45
i just want to set the scene really because i think without setting the scene people might not really appreciate
2:52
um the exciting data the landmark data that i'm about to share with you
2:59
glioblastoma is a very aggressive primary brain cancer
3:04
it hasn't so far responded well to immune therapy it's classed as being
3:11
immunologically cold it's a very difficult tumor when you look at it genetically is extremely
3:18
heterogeneous and and then very very able to change
3:23
and evolve and debate treatments it's got a very invasive phenotype
3:29
and the recurrence rate is approaching 100
3:34
if not 100 it's universally fake really
3:40
the standard of the care is to have surgery and it's not possible to take all the tumor
3:47
out due to the glandular stoma being such an invasive tumor there are always cells left behind
3:54
and there's always recurrence unfortunately however the more tumor that's removed the better it is for the
4:00
patient's survival so following surgery in standard of care there's six weeks of radiotherapy that's
4:07
monday to friday on the brain five days a week 30 treatments along with chemotherapy and
4:15
then six months of more chemotherapy it really is quite a
4:20
grueling punishing schedule the treatment to have all that radiotherapy and chemotherapy
4:29
and however unfortunately it does not give them so much survival advantage so even with all of that
4:36
treatment the average survival is around 15 to 17 months and
4:43
tumor recurrence occurs within the first year and then um the median overall survival
4:49
from recurrence is six to ten months and when you look at what we might call
4:55
long-term survivors which we clusters um five years in glioblastoma that's actually only five percent
5:02
so it really is a very difficult disease and then the question is well what's
5:09
been done about it well there has been a lot of clinical trials in this area there's been if you
5:15
look at this publication um from 2016 2018 sorry there are
5:22
417 clinical trials for glamostoma and this included nearly 32 000 patients
5:30
and of all of those trials including 16 very big expensive phase iii trials only
5:38
one showed evidence of efficacy and that was the truma treating fields device
5:46
but since then there's been more failure in glioblastoma so it really has been a
5:52
real battleground filled with lots and lots of failure
5:58
um the when we look at the actual treatment itself the um treatment originally was
6:05
surgery and radiotherapy and in 2005 um it was shown um that
6:12
um from a large phase iii study that by the addition of chemotherapy temozolomide there was an addition of
6:18
2.5 months this actually was really um
6:23
groundbreaking at the time because it showed that actually chemotherapy could make a difference to glioblastoma and we
6:30
were very hopeful at this time that actually we could then improve outcomes
6:36
but to date we had not um and there was um
6:42
been no real change um aside from um this in the last 17
6:49
years and there were there was some data from glioda wafers and these are chemotherapy
6:56
wafers that are put in with the during the surgery they're not generally used they um they are um don't have much
7:04
efficacy and that they're not very um they're not very popular to use
The Trial
7:10
but i'm pleased to tell you so that we've um i'm gonna share with you the results of the dendritic cell dc
7:17
space 3 trial and when we look at the trial itself what happened for these patients was
7:24
that 331 patients from 94 trial sites in
7:29
four countries were recruited and the patients were all patients with newly diagnosed climbing stoma
7:36
the patients had surgery and then the tumor tissue was taken and sent off to the
7:44
laboratory and following this the patients had leukopheresis
7:50
and with this they were able to manufacture dendritic dendritic cell vaccination therapy
7:58
the trial was a double blind randomized trial
8:03
and importantly it had crossover the trial began a long time ago now back
8:10
in 2007 and enrollment was suspended between
8:17
2008 and 2011 and the reason for the suspension was
8:24
nothing to do with safety or any of the reasons it was actually purely for financial reasons
8:29
but fortunately the trial was opened up again and it was um
8:36
investigators were very enthusiastic to be part of the trial and from 2012 to
8:42
2015 92 percent of the patients uh were enrolled in this study
8:48
with the last patient being enrolled in november 2015 and with this trial it's been important
8:55
to wait for the long-term survival of data so as we can see what effect the immunotherapy has over a long period
9:03
because it's actually within the therapy we're looking for what it does to that proportion of patients
9:08
and their long-term survival so this shows the screening and the
9:14
enrollment and it was actually a very straightforward study for us to um
9:21
to treat patients um the patients were screened they were
9:26
enrolled they had their surgery the tumor tissue was taken it was sent off to the laboratory and then the
9:33
leukophresis was done three weeks after the surgery whilst the patient was undergoing chemo
9:38
radiotherapy there was manufacturing of the dendritic cell therapy and then when
9:43
this was completed the patients then had the autologous dendritic cell vaccination
9:50
just as a intradermal injection into the arm treatment was given alongside the
9:57
standard temozolomide chemotherapy and depending on how much vaccination they was able to make
10:03
and patients had treatment at day zero day 10 day 20 months 2 4
10:10
8 and 12 and then every six month thereafter i have to say from my experience the
10:17
treatment was extraordinarily well tolerated and i saw no side effects in
10:22
any of my patients the trial was a crossover design
10:28
and the reason for this was because at the time it was not considered ethical for
10:35
patients to undergo leukopherosis which is invasive and then
10:41
not have the opportunity to have the vaccine at some point so um it was
10:47
extremely important that this was included and
10:53
and but this did create difficulty later on and also opportunity later on
11:00
um the original therefore the original primary endpoint when the trial was designed was
11:06
progression-free survival and at this time when i think back to then we weren't
11:13
really aware of this concept of pseudo-progression and pseudo progression is something that
11:20
we see and we recognize very clearly now and it occurs with immunotherapy but it also
11:26
occurs when patients have radiotherapy antennas on my chemotherapy and so what happens here is that
11:33
patients have the treatment and then if you do a scan at the end of the treatment it looks like the tumor's
11:39
grown but in fact what you're seeing is swelling and dead tissue and tumor
11:45
infiltrate with um lymphocytes and actually there's a response to treatment
11:51
and these patients generally do better when they have pseudo progression
11:56
so therefore at this time we didn't have good imaging to differentiate tumor
12:02
progression from similar progression which we do now
12:08
so um so that's why the progression-free survival needed to be removed as the
12:15
primary outcome measure um and in fact this is the results from
12:20
the progression-free survival which isn't very surprising so when you look at progression-free survival and there
12:26
was no significant difference between the two patient groups
12:33
however when we look at overall survival um which is obviously what's most
12:38
important and the um this was made the primary
12:44
endpoint in the study and included in the statistical analysis plan
12:50
prior to the underlining of the data um
12:56
so when we look at this sap we see that the primary endpoint was
13:01
overall survival in the newly diagnosed glioblastoma patients
13:06
so and what they've done is they've looked at external controls for this study
13:12
because 90 of the patients in this study ended up receiving the vaccine
13:20
which you'll see was actually very important for the patients for the recurrent disease and i'm very pleased
13:27
that they were had the opportunity to have the vaccine so
13:32
232 patients of the 331 patients
13:38
had um had the standard treatment plus the vaccine
13:44
at newly diagnosed however at crossover 64 patients of
13:50
recurrent disease also then had the vaccine so we have the data for the survival for the newly
13:57
diagnosed and the recurrent patients but this then means that we need external controls for the newly
14:04
diagnosed and the recurrent patients so the external controls needed to be
External Controls
14:12
sourced and validated and needed to be done independently of the sponsor
14:19
so an independent expert firm was appointed
14:24
to evaluate um other glioblastoma patients and that were treated in clinical trials
14:33
and they were given a criteria to match very closely with the patients
14:40
in this particular study i'm just going to show you very briefly
14:46
how the validation was done but not discussing in detail
14:53
and when we look at the external controls we can see that these are very well
14:59
known and very accepted publications that were used for the external controls
15:05
for the newly diagnosed blastoma patients and also the external controls
15:10
for the recurrent patients and you can see how well these patients are matched
15:17
and this data will be available later for people to scrutinize um but i'll just
15:23
show it very briefly
Study Results
15:29
so now we come to the most interesting part of the talk which is actually the study results
15:35
so i'm very very happy to say that the primary endpoint the media notes of our
15:41
overall survival in newly applied diagnosed fibroblastoma patients reached
15:46
statistical significance as did the secondary endpoint that is that patients
15:52
with recurrent disease who had dendritic cell therapy
15:57
had improved survival the safety profile was excellent
16:03
there was two thousand to 193 doses of dc vacs administered
16:09
only five adverse events were reported and no significant
16:15
immune reactions so the important landmarks are
16:23
that the median overall survival for patients with newly diagnosed
16:28
glioblastoma was 19.3 months from randomization and 22.4
16:35
months from surgery and this is versus 16.5 months that you would expect
16:40
normally and was seen in the randomized controls
16:46
and the methylation of mgmt which is a good
16:52
prognostic marker for these patients showed a very enhanced survival of
16:59
30.2 months from randomization versus the normally expected 21.3 months
17:06
and what was extremely impressive is that the survival of five years in
17:11
these patients is 13 versus 5.7 percent
17:18
then when we look at the recurring glioblastoma the median those raw survival was
17:24
extremely impressive as showing a 13.2 months median overall survival
17:31
as opposed to the 7.8 expected
17:36
median overall survival and even here we see a survival tale at 24 months we see
17:45
of patients alive and at 30 months 11
17:51

of patients alive and at 30 months 11
17:51
which is much better than you would expect for these patients
Innovation
17:58
so there's been innovation in this trial and this had to come about because
18:04
um the um because of the crossover design that was
18:09
required in this but this is the first phase three trial of a
18:15
systemic treatment in 17 years to show significant extension of median overall
18:21
survival in newly diagnosed fibroblastoma and the first phase three trial of any
18:28
treatment in 27 years to show a significant extension of median overall
18:34
survival in recurrent glioblastoma these are extremely important statements
18:41
and are very very exciting and really important for this patient group
18:48
and what is particularly important that this is
18:53
this phase three trial shows meaningful increases in long-term survival both in
19:01
newly diagnosed and recurrent glioblastoma
19:08
what's interesting in with this particular treatment is it's has no
19:13
little or no toxicity and it really is suitable for combination with a wide range of other
19:21
treatments which people can spend a lot of time thinking about chairpoint inhibitors
19:26
oncolytic viruses cytokines chemotherapy etc
19:32
and and what's really also really exciting is with this particular technology is
19:39
that when the patient recurs and they have further surgery you can make a new batch of this treatment and
19:46
so the target so this tumor evades um and treatments because it changes but
19:53
you can actually just change the treatment with the tumor and potentially um
20:00
this works in glioblastoma so actually it can actually work in other tumor types so it's really a very very
20:08
exciting technology and this slide just looks at how it can
20:15
be combined and what people can do with it in the future
Survival
20:20
so this shows the overall survival gap in my curve in
20:27
the newly diagnosed patients and you can see this is very very favorable and you can
20:34
see very clearly the um that there's no crossover and you can
20:39
see the long term survival which is very impressive for this group of patients
20:47
so these are the important landmark survival rates in the newly diagnosed
20:52
patients so um at 36 months you have a 20 survival
21:00
48 months 15 and 60 months five years over 13
21:06
survival as compared with what you'd expect normally of around five percent
21:14
and when we look at the subgroup analysis you can see here that actually in every
21:21
subgroup analysis there's a favorable outcome so when you look at age
21:28
and residual disease and when you look at this particular marker which is a gene called
21:34
mgmt that when it's methylated the patients have a favorable outcome but
21:39
you can see it's much more favorable when they have um this um treatment
21:46
so this is looking at newly diagnosed glandular stoma and this morning this is the first time that i've
21:53
seen this slide and i'm really very very intrigued and very excited that this
21:59
shows that this technology which is extraordinarily well tolerated
22:05
um is showing an increase in survival in patients over 65.
22:12
and you're showing long-term survival in this patient group and when we look at the under 65s these
22:20
people have a better prognosis generally but actually with this technology it's actually improved further
22:28
and then when you look at this very poor prognostic factor of significant residual disease
22:34
this is really impressive you're seeing that this this this technology this
22:39
dendritic cell therapy is impacting on this patient group in a way that i would not have predicted
22:46
so it's really very very interesting and when you look at the minimum the
22:52
patients with minimal residual disease there's always there's also an advantage
22:57
in survival there and this is the methylated groups of
23:02
this is people with the favorable gene configuration of methylated promoter
23:08
region of mgmt and when you look at the five-year survival in this group it starts to look
23:14
really interesting and really there is nothing that could
23:19
have predicted this survival in this patient group and it's so impressive
23:26
and this is the patients who've got a very poor prognostic marker of unmethylated promoting region of mgmt
23:34
but even they have a survival advantage even though it's smaller
Recurrence
23:40
then we come to the recurrent landless department where really very little makes an impact and i would not have
23:47
anticipated that these patients would have had an impact with dendritic cell therapy
23:53
but actually when we look at the overall survival in recurring clioblastoma you can see the survival and if you treat
24:00
this condition you'll see that that is a very favorable survival curve for
24:06
recurring limelastoma we're seeing 13.2 months median overall
24:12
survival and we're seeing entail a survival tale that goes out to five
24:17
years and here we can see
24:22
the landmark data so incline recurrent cloud blastoma six
24:27
months is a landmark because people aren't expected to make it six months
24:33
but with with um dendritics of a dc maxell their survival is 90
24:39
and at 24 months 20 survival which is really very very
24:47
impressive and at 30 months we're seeing 11 survival
Therapy
24:54
so dangerous itself therapy how does it work um i think that this audience is
25:00
probably more familiar with that than a brain tumor audience so it uses the
25:06
master cells of the immune system the dendritic cells to mobilize
25:11
multiple elements within the immune system the technology that's used
25:16
in manufacture of dc vaxelle is fully personalized
25:22
um it inherently targets antigens which are actually on the patient's tumor
25:29
and fits the patient's version of the cancer so it really is a personalized
25:36
vaccine and unlike other technologies um it uses
25:43
all of the tumor antigens not just um some manufactured peptides
25:50
or it it makes and this makes it difficult for tumors to mutate around the antigens
25:56
that have been targeted so this just shows um a slide on how the
26:04
dendritic um autologous dendrites does work
26:11
and how they multiply and activate these t cells
26:18
and this is just a slide so there's actually a lot of evidence that
26:23
t-cells cross the blood-brain barrier both in animal models and also now in
26:30
them in humans and this is some unpublished data from linda liao
26:36
which shows infiltration of t cells into glioblastoma tumor into collaborative tumors in patients
26:42
who were treated with dc max l so in conclusion
Conclusion
26:48
um the comple this is shows the completion of a large phase 3 trial including 331 patients
26:56
it was really a mammoth effort over many years and i was very very honoured to be part of that
27:03
journey with all my co-investigators and with northwest bio um there was 94 sites
27:11
70 clinical investigators four countries and i think it's very exciting that
27:17
we're seeing practice changing results not only in newly diagnosed glioblastoma
27:24
but also in recurrent collaboration i can say from personal experience that
27:29
this vaccine is um easily administers and it has a very very favorable side
27:37
effect profile and the the use of these external
27:43
contemporaneous clinical trials is innovative and i think it's been really
27:49
important for this particular trial because the patients in this study
27:54
have recurrence had the vaccine and the vaccine was effective that actually we
27:59
need these um external controls um
28:06
and what's particularly significant is that there is a significant percentage of long-term survivors
28:11
and that's consistent with immune memory effect by the t cells and this really
28:17
can change the natural history of glioblastoma and i don't think we've really seen that with any other
28:23
treatment and we're still looking at the data on this
Longterm survivors
28:29
and i've only seen some of this data this morning and i'm really quite overwhelmed by it that we're seeing
28:35
some populations that i wouldn't have anticipated to see um benefit or seeing old patients
28:44
patients with residual disease and doing really well with this
28:49
treatment which is really quite um dramatic
28:54
so this treatment is really feasible and because there's so there's no side
29:01
effect profile or very little side effect profile and it really is possible
29:06
for this to be rolled out as a treatment around the world
29:12
and thinking about how we can use it going forward of course we need to think about
29:18
combination treatments and we also need to think about what is this
29:23
how is this changing the immune micro environment and more work is ongoing in that and
29:29
i think it's a very exciting area of research so in summary i can say that patients
Summary
29:38
with treated with dc maxell show the clinically meaningful and statistically
29:43
significant extension of survival in both newly diagnosed and recurrent glioblastoma
29:50
patients have an excellent safety profile and it's really noteworthy to
29:55
see these long tales of survival so i'd like to
Thank you
30:01
thank um linda liao for giving me the opportunity to speak to them sorry that she was unwell to miss the talk and i
30:08
know that will um be of regret for her and but also to dr robert prince who led the study
30:16
from ucla and to my colleague professor ashkam at bing's college and to all um
30:22
my colleagues who are investigators and sub-investigators and the trusted steering committee and of course to all
30:29
the patients and their families who participated in this landmark study
30:35
so i'd be very happy to answer some questions now if anybody has any questions
Questions
30:43
well thank you very much for a very very interesting presentation congratulations on the survival benefits that you've
30:50
seen in these patients uh the floor is now open for questions we're gonna do about five minutes worth of questions so
30:58
david hi hey paul is dave reardon from boston congratulations uh really wonderful
31:04
study and great work um could you comment on what was known about idh status of the
31:10
patients who enrolled what about steroid use for patients who enrolled
31:15
and why you might anticipate the unmethylated patients didn't benefit
31:21
was there maybe some synergy with chemotherapy that really caused immunogenic cell death and enhanced
31:27
you know antigen priming or some other reason why the patients who got chemo seemed to have a preferential benefit
31:34
yeah it's really quite um interesting that so the idh status of course it
31:39
wasn't stratified for them because we didn't have the idh status for the patients largely at that time but we do
31:46
have the um data on the steroid use but steroids
31:51
were and permitted in study but they were um limited to less than four milligrams
Unmethylated patients
31:58
um and the um and then the question about the unmethylated patients it really is
32:04
interesting and i think you're quite right that's the conclusion that we've drawn that there
32:10
must be some synergy um with the temozolomide where the temazonomide is
32:15
active in these patients but um yeah it's interesting and i'm not sure that we can explain all the results but it's
32:22
great to see them and david marnix bosch from uh in by i would like to add something in
IDH mutations
32:28
that answer yeah thanks and and thanks for the question um actually the number of idh mutations
32:34
was i think seven patients out of 331 and which is lower than what you saw in the in the comparator groups
32:41
um so that that doesn't uh contribute to the results that we're seeing um the question about methylation for
32:48
sun methylation i think is very interesting and sort of raise the speculation as to how this treatment can best be combined with other treatments
32:55
um but an answer is death will be more speculative than anything else and right now it's an interesting observation i
33:01
agree with you and you know the study as you indicated paul he really is quite innovative and
33:09
sets a potential precedent for the use of these external control groups which many
33:14
studies are now incorporating to a degree and will make randomized trials much more
33:22
much more easy to do much more readily doable but was there any kind of validation i wonder within the study of
33:30
patients who enrolled just to show a survival benefit of the
External control group
33:37
outside of the external controls because usually when we bring external controls in there's kind of an internal
33:44
group of controls where there's a validation and then you expand that with the externals
33:49
here the control group is really consisting exclusively of the
33:54
external control so for example for patients who progressed
34:00
who got vaccine versus those who didn't was their survival benefit
34:06
for uh the patients before crossover or or amongst the patients who didn't
34:11
cross over maybe it was any kind of a it was could you tease out anything from the internal control patients
34:19
um to support the results for the external control validation do am i
34:25
making that clear at all i think i think a bit maybe my next stem
34:31
if you could comment on that
External control validation
34:42
there was quite a bit of validation of the external controls actually um one thing we did is we compared the
34:48
treatment arm of all of the trials that were selected for comparison against the external controls and asked the question
34:55
whether the results compared to external controls in those trials were consistent with the ones that were originally
35:00
observed for those studies and as you know almost all of those studies except to one disto trial for
35:06
the optune device were negative and if you compare the treatment arms of those studies to the external controls
35:13
you get exactly the same result so i think that's a very important comparison
35:18
and another thing we did several sensitivity analyses um we um
35:25
we did what's called an maic which is uh adjusted independent compare indirect
35:30
comparison where you um even more closely then so the populations were
35:36
already quite well matched in terms of prognostic factor and demographics but they're never perfectly matched but you
35:41
can then go back and more and better match your population to the control population which reduces statistical
35:48
power and but if you do that then you still maintain a significant um positive
35:53
outcome and in the comparison and then there was another series of uh
35:58
sensitivity analyses that we did and just to give you an example one is the called leave one out analysis where
36:05
subsequently you remove one study from the external control cohort and again
36:10
the results were completely identical then there was one other um test that we
36:16
did because two of the trials did not specify clearly two of the comparator trials and newly diagnosed ubm the two
36:22
gilbert trials did not specify specifically whether they removed patients with recurrent disease and from
36:29
eligibility for current disease early recurrence at post chemo radiation so we
36:34
removed those two from the comparison as another sensitivity analysis that also did not change the result so this just
36:41
gives you a sense of the rigor that we went through to to validate these comparisons thanks for your question
External control data
36:49
thank you alex hi um really interesting to see you've got
36:55
data from external controls here a question i have is i see there was about 1400 patients in your external
37:02
control did you find that you had any non-missing data from all the 1400
37:08
patients which is what the fda generally requires um
37:14
we were of course dependent on what was published and so you extract individual patients you
37:20
reconstruct individual patient data from the published kaplan-meier plus now fortunately those trials were
37:26
described in very great detail and both including demographics etc so i think in
37:32
terms of the quality of the comparison cohort it really couldn't have been any better um which was really the result of
37:39
the other studies that were really well executed so this was mostly a comparison
37:44
to a historical control rather than individual patient by patient matching using propensity scoring or statistical
37:51
analysis well there was no propensity scoring because for that you need actual independent
37:56
actual individual patient data and those have not been made available for comparison and i think that's something
38:02
that we should all stress in the future that that actually should be done so these trials can be um
38:08
even more rigorous than they already were um i wouldn't call them historical controls because they were from contemporaneous
38:14
trials they were conducted at the same time roughly in in comparable institutions of the same quality
38:20
and with very much the same parameters um so that i think again underscores the
38:25
validity of this approach thank you and i said that wait
Site of vaccination
38:34
uh clarifying question about cytovaccination this is subdermal or
38:39
intradermal vaccination right not intra-tumor okay and and do you there's potential
38:46
because the site of vaccination is very important on whether it be oncolytic viruses or dendritic cell vaccines
38:52
what's your thought on what your future would be yeah we had a lot of talk about that and we
38:57
put this in the upper arm sort of thinking in a very simplistic way that the closer you put it to the
39:03
tumor the more effective it will be but often i say you can probably put it in the big toe and it won't make any
39:08
difference as long as the neutral cells can get to a lymphoid organ probably a lymph node where they can interact with
39:14
t cells those t cells travel anywhere through the body and they actually make it to the tumor sites no matter where
39:19
they are induced because we have we had talks about intra-terminal injection other vaccines
39:25
and that's that looks like a palatable pathway and that will be a completely different presentation
39:35
one more uh let me i'm megan do you have any from outside from virtual
39:41
well let me do that first steve i'm sorry give them virtual attendees a chance
39:56
wait could you turn the microphone on
40:07
okay um the most popular question from the virtual audience is what is the process
40:12
for fda approval now
Most popular question
40:17
we we really can't speak to that it will be no different than for any other treatment
One more question
40:24
one more question yeah i wanted to uh answer david's question um
40:30
and uh congratulate paul holland and the northwest bio team without being
40:36
self-congratulatory my full disclosure i'm one of the 70 authors
40:41
and we've been waiting for uh advanced like this for a long time david in addition to the
40:47
external controls and the numbers um we have some unpublished data from pan
40:53
uh dr mohan's team has been looking at radiological markers and we'll present that in june and that's obviously uh
41:00
will add to the story uh in terms of using each patient as a control and
41:06
and having uh another dimension of efficacy thank you
41:13
all right thank you very much sorry i went over a little bit on time but i think this is an important uh presentation
41:19
that generated very interesting questions so now we move forward with another virtual presentation
41:26
um peter sorger professor of systems biology at harvard medical school head of harvard program
41:32
in therapeutic sciences i see he's ready to go he's going to speak on independent drug action immunotherapy implications
41:39
for drug discovery and precision medicine peter