I will dig though these transcripts and try to pie
Post# of 148190
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Posted On: 02/28/2019 12:20:32 PM
I will dig though these transcripts and try to piece mono discussion together.
Here is NobelCon15 transcript on January 28th
00:03 thank you everyone for being here for
00:05 Saturday and presentation excited on our
00:10 lead product is liran Lima Pro 1:40 we
00:16 are developing Lear on the map for HIV
00:18 and cancer I will be making
00:21 forward-looking statements
00:26 biotechs are usually when there have a
00:29 stock price below $1 they call them
00:33 high-risk high-reward I'm going to make
00:37 a case today that we are low-risk
00:39 high-reward
00:40 the reason for that is we had our
00:43 primary endpoint I mean it's all about
00:46 getting your phase 3 completed we
00:48 completed that and we have done much
00:51 more than that so I believe it's
00:53 low-risk high-reward we started
00:57 developing this product for HIV our
01:01 first phase 3 pivotal trial is a world's
01:05 first self injectable product for
01:08 patients who could die if they don't
01:12 have this product HIV does not kill
01:15 anymore there are products that will be
01:17 able to make this deadly disease a
01:20 chronic disease but not for this
01:23 population this population patients that
01:25 have three or four classes resistance
01:29 they have AIDS
01:30 so we're not talking about a population
01:33 that's just the normal population it's a
01:35 population that you are in great need of
01:38 this product so this is a first self
01:41 injectable antibody for that population
01:44 the unmet medical need population we
01:49 also have another phase three that one
01:52 is not a pivotal trial that one's going
01:55 to need a pivotal trial after it's
01:57 completed the reason that trial was
02:00 going on is because we have a lot of
02:01 interest on this product for mono
02:04 therapy Gilead and viv are working on
02:10 the next generation of products for HIV
02:12 they've developed two
02:16 two component product for HIV all the
02:22 HIV products are three component if they
02:25 don't have three component they're not a
02:27 regimen that can stop HIV from killing
02:31 we've developed a product with two
02:33 components they spent several hundred
02:36 millions of dollars this trial is a
02:39 single component one product
02:42 it's not even synthetic drug it's
02:44 humanized monoclonal antibody we have
02:49 patients who were taking four or five
02:51 pills a day three pills a day an exact
02:53 time they had to take it because if they
02:55 miss a dega resistance resistance is
02:57 dangerous in the world of HIV and they
02:59 have gone four years some of them four
03:02 and a half years without any standard
03:05 care pills just simple injectable sub-q
03:09 at home once a week 30 seconds and
03:12 they're done so that's our HIV story the
03:17 next one is graft-versus-host disease we
03:20 were surprised when Pfizer came back
03:22 came out and says our HIV product has
03:25 indication in GVHD leukemia patients who
03:28 need bone marrow transplant so we did in
03:30 vitro study ten thousand dollars cost
03:32 the study FDA gave us Phase two skipping
03:36 all the development that's how much FDA
03:40 thinks of this product that's what we
03:42 have fast track designation that's what
03:43 we got twenty eight million dollars
03:45 water grant from NIH at the early time
03:47 but this product was being developed
03:50 tnbc triple negative breast cancer now
03:54 waiting to cancer world-renowned
03:57 oncologists figured out that there's
03:58 another use for the mechanism of action
04:01 for HIV product that are ccr5
04:04 antagonists we're going to get to that
04:06 that's our very important study colon
04:10 cancer Phase two we want to be not in
04:12 Phase two we want to file an IND
04:13 initially drug application for FDA to
04:16 give us another Phase two for another
04:18 indication and prognostic tests we'll
04:21 talk about that we like to get approval
04:23 for that this year hopefully we're going
04:25 to talk to FDA all the studies have been
04:27 done so what's the mechanism of
04:31 this product that has so many potential
04:34 perhaps next Humira if you look at if
04:39 you look at the cell HIV doesn't kill
04:44 anybody if it doesn't intercellular you
04:49 get a flu you find if it doesn't enter
04:52 the cell our product stops the virus
04:54 from going into the cell before the
04:57 whole thing starts it stops it and
05:00 here's a magnified picture of the
05:04 membrane there's two receptor cd4 ccr5
05:08 dr. paul madden invented I mean
05:10 discovered that HIV has to interact with
05:13 this receptor and then this one to get
05:15 in there so he invented through one
05:18 fully round him a pro 140 he discovered
05:21 that dr. Richard pastel on the other
05:23 hand discovered that there is another
05:25 use for this and octopus sir will had
05:27 address you about the potential other
05:29 potential of this product so at the
05:33 early time when this product was being
05:36 developed to 12 years ago FDA gave it
05:41 fast track designation stating that
05:44 there are clear advantages of leer only
05:48 map where it says current standard of
05:50 care we have a letter from FDA says you
05:53 got fast track designation and these
05:55 were the reason they cited twenty eight
05:57 million dollars from NIH was given to
05:59 this product I get the last six million
06:02 dollars back to NIH because I thought
06:04 that this product has a lot more
06:06 potential than just going after
06:08 substance abuse population that was five
06:11 years ago today I'm proud to say that
06:14 that was a good path we took here's our
06:19 first combination therapy 52 patients
06:23 were there because this is unmet medical
06:25 need population primary endpoint hit
06:28 p-value point zero zero three eighty one
06:31 percent of the patients who never some
06:34 of them never could have suppressed
06:35 viral load suppressed viral load means
06:38 you don't chance meet HIV to somebody
06:42 else very crucial for other
06:44 not just for the patient alone 81% had
06:48 suppressed viral load we have letter
06:50 from a physician saying my patient for
06:52 27 years didn't have suppressed viral or
06:55 do not take this patient already pro 140
06:57 at the end of the study so we didn't
06:59 either had 45 percent for 48 weeks we
07:03 had eighty one percent I believe zoom at
07:06 last product got approved forty three
07:08 percent for 24 weeks we never had any
07:11 serious adverse event with this product
07:13 for the last 670 patient that is related
07:16 to pro 140 later on Lima we don't this
07:19 product is safe this product is really
07:23 stated about state about so 40 patients
07:27 from this population is still I went to
07:30 the extension we still have close to 30
07:33 patients in extension some are gone for
07:35 three years close to three years now
07:37 three years regulatory pathway we met
07:40 with FDA we are carefully crafting a
07:44 press release to come out about our
07:47 meeting with FDA just last December just
07:51 last month we we had a conference call
07:53 with FDA to fine-tune our BL a biologic
07:57 license application I'm very excited
07:59 about that and we will be looking at FDA
08:02 minutes to just make sure that we
08:04 reflect exactly what we got we are this
08:06 far away from approval so we want to
08:08 make sure that we indicate to everybody
08:11 what's happening these last few weeks or
08:14 months before we get to the submission
08:16 of B la mano therapy we also discussed
08:21 that with FDA we will be putting out
08:24 press release about that also our
08:26 responders rate in the past was said to
08:28 be 90% 700 milligrams we will be update
08:30 you get you everybody about that but we
08:33 have a path to approval now we got there
08:36 high responders and we set out so many
08:39 things to do
08:39 done every one of them and we're
08:42 successful in every one of them having
08:45 failed in combination therapy primary
08:47 endpoint haven't failed on finishing the
08:49 trial with a great result haven't failed
08:51 to get mono therapy to the finish line
08:52 we have a fail to find out other
08:55 indication for this product so
08:58 to that let's look at the market size
09:00 for combination therapy I'm gonna go
09:03 with this slide we had a hard time
09:05 pricing this product before we put lower
09:07 price here but then well as we are
09:09 talking right now with Big Pharma which
09:11 we said to everybody we're talking to
09:12 Big Pharma's we realize if we priced it
09:15 for HIV one price and for cancer and
09:18 other one is going to be disaster
09:19 getting this license for each indication
09:22 so what we did is we put a $70,000 price
09:25 the current product for HIV unmet
09:29 medical need is selling from 100 $18,000
09:32 per patient per year current antibody
09:35 for cancer is selling for $70,000 per
09:39 year per patient so we'll go with 70s
09:41 Devi that with all the indication that
09:43 we might have the market size for this
09:45 combination therapy is pretty
09:47 significant and for mono therapy is much
09:50 higher this is the report from
09:54 independent report by Ovid going to the
09:57 patient's doctors to payers and they
10:00 said that one of the things that they
10:01 said is 95% of HIV patients said they
10:04 would have no problem using this
10:06 injectable they're not going to worry
10:08 some big formal says hey they might not
10:10 take injectable big for most we said no
10:12 here it is 85% take it no problem from
10:16 mono therapy 95% for combination so that
10:20 concludes everything about HIV what we
10:23 were shocked when Pfizer comes back and
10:25 says this product has their product the
10:28 ccr5 antagonists which got approved
10:30 maroc has a blackbox warning has side
10:32 effect has to be taken by patients twice
10:35 a day pills this is not that so that
10:38 product is not comparable ours we did
10:42 GVHD we compared our self Tamara Brock
10:44 in in vitro study we had good results so
10:47 we went ahead and sent that results to
10:49 the FDA we got phase two when I asked
10:52 for orphan drug designation the FDA says
10:54 take two groups of 32 miles inject all
10:57 of them with human bone marrow if all of
11:01 them died then that means you know human
11:04 bone broke kills the mice but give half
11:06 of them near on the map if some of them
11:09 are stay alive
11:10 you got yourself orphan drug
11:11 nation 100% of the mice stayed alive a
11:15 hundred percent of the other mice died
11:17 because it's a hundred percent we did it
11:20 again and again and again and a result
11:23 same saying the mice that had no Lear on
11:27 the map their weight loss was drastic
11:29 night and day so we got off on drug
11:32 designation then that's when we got
11:35 shocked when we hear dr. Richard pastel
11:38 500 patients pay per published in
11:41 peer-reviewed journal I published one
11:43 paper I got my PhD in mechanical
11:44 engineering we did 500 so figure it out
11:48 he comes to us and says I discovered
11:52 something I discovered and I published
11:55 it that the metastasis of cancer that is
11:57 responsible for killing mankind can be
12:00 stopped by your product now when you
12:04 find something like he did you don't you
12:07 can't do anything with that you gotta
12:09 have a product that does that so Pfizer
12:11 and marek approached him they did this
12:14 study
12:14 he holds the patent now we hold it
12:16 because we acquired his company but then
12:19 he didn't like Pfizer and where he come
12:21 to us he said yours doesn't have any
12:23 serious adverse event or toxicity that
12:27 is comparable to Maryborough it's hardly
12:29 any toxicity or side effect so I wanted
12:31 I want your product we said we don't
12:33 have any money he said we don't want
12:36 money we want shares of your stock
12:39 that's a valuable valuable commodity and
12:42 we did the deal so sure so we have the
12:46 brain trust in our company now he talks
12:48 about his discovery that needs our
12:52 product so we have patented everything
12:54 and it's been almost honor for me to
12:58 work with this gentleman and I'm very
13:00 pleased to introduce him so he can
13:02 explain everything doctor person well
13:07 good afternoon everybody can you hear me
13:09 up the back I'm very pleased to be here
13:12 today and to be involved with cider dine
13:15 at this pivotal moment in their history
13:17 I'm relatively new to the company
13:19 compared to most everybody in this room
13:21 we formally sold our company didn't
13:25 member 2018 and a lot has happened the
13:28 last couple of months I thought I'd
13:30 share with you a couple of insights
13:32 related to how and why the company has
13:36 pivoted from HIV into cancer in a
13:40 nutshell nada shared with you that
13:42 sighted on is a publicly traded company
13:45 that is on the OTC as a market cap of
13:48 around hundred fifty five million that
13:50 has successfully completed a phase three
13:52 study for HIV having met all its primary
13:55 endpoints that's currently conducting
13:57 its PLA and is a highly de-risked
13:59 company in that context my laboratory
14:03 about seven or eight years ago had been
14:07 investigating the mechanisms by which a
14:10 cancer cell metastasizes and at that
14:14 time it really wasn't understood exactly
14:16 how that happens and it's the spread of
14:19 cancer that kills people now to mention
14:22 to you today that there's a receptor
14:24 called ccr5 which is essential for entry
14:27 of HIV into the t-cell that ain't what
14:31 it usually does okay what what CC r45
14:35 normally does on it on a t-cell is to
14:37 direct its movement so when a t-cell
14:41 activates ccr5 or its ligand it moves so
14:45 one of the normal functions of immune
14:46 cells they're policemen of the body
14:49 tracking down infections and
14:51 inflammation and the cell moves because
14:54 of the ccr5 pressed on cell surface now
14:59 we found that surprisingly when we use
15:03 an artificial intelligence approach that
15:05 cancer cells turn on that same receptor
15:08 and when a cancer cell does that it
15:10 starts moving so we showed that this
15:14 receptor normally expressed just on T
15:16 cells promoting migration to the bones
15:19 and brains the other place where immune
15:22 cells go does the same thing for a
15:24 cancer cell so the ccr5 is necessary and
15:28 sufficient for the movement of cancer
15:29 cells to the bone to the brain to the
15:32 lungs and other tissues
15:34 now note i had mentioned what we had
15:38 which was to study a variety of
15:40 different cancers and I'm going to show
15:42 you some primary data but just to
15:45 preempt it we looked at 2200 patients
15:48 with breast cancer we look at every gene
15:51 in their cancer and we found that about
15:54 50% of breast cancers overexpress ccr5
15:58 50% so the previous blockbuster which
16:02 was Herceptin targets about 12 to 15% of
16:06 human breast cancers but unlike
16:08 Herceptin ccr5 is turned on in other
16:11 cancers it's turned on about 50% of
16:14 prostate cancers pancreatic cancer colon
16:17 cancer variety of different types of
16:19 metastases I was particularly struck by
16:23 colon cancer both my parents died of
16:27 metastatic colon cancer and you know my
16:31 father was a cancer surgeon he was here
16:34 at SLU who's at sloan-kettering and
16:36 ultimately moved to Australia to Perth
16:39 big guy six foot two high jump champion
16:41 sprint champion and when he had
16:44 metastatic colon cancer he he couldn't
16:46 stand up to take a pee so this is a
16:48 disease that brings a strongest man a
16:50 woman to their knees so when we found
16:52 that there was a receptor which was
16:55 targetable that was driving that
16:57 metastatic process I was very excited at
17:01 a very deep level about the potential of
17:03 shifting this game in in the cancer
17:05 metastasis field thank you
17:14 excellent
17:18 so this is some of the the primary data
17:21 and this is a study with 2200 patients
17:27 so patient one two three four to 2200
17:30 and this is every gene in their cancer
17:33 and this arrow means this is ccr5 and so
17:37 ccr5 is turned on where it's red so all
17:40 these patients have ccr5 turned on the
17:44 cancers to these other patients but I
17:46 was very focused on this group of
17:47 patients because triple negative breast
17:50 cancer is a terrible terrible disease
17:52 now I've been looking after patients for
17:54 nine thirty years and triple negative
17:56 metastatic triple negative breast cancer
17:58 typically kills a woman within nine to
18:01 ten months at the time they appear in
18:03 your office typically attacks Eskenazi
18:06 Jewish women women of that descent
18:08 African American women and we currently
18:10 don't have any targeted therapy the
18:15 standard of care is chemotherapy and
18:17 surgery so identifying this as a
18:20 potential target ccr5 and all these
18:23 women was very very exciting and this is
18:26 I hope you can see this these are the
18:28 breast cancer cells here and this is
18:30 their their metastasizing in this case
18:32 they're invading through Maitre gel and
18:34 this is at their journey and here you
18:37 can see we had Lauren Elam AB Pro 140
18:39 when we used this small molecule on here
18:42 but we dramatically cut that invasion
18:45 and Stokes dependent we upped the dose
18:46 we block the the invasion and metastasis
18:49 now nada had intended to mean that when
18:54 I had used the Merck and Pfizer drugs I
18:57 had demonstrated that they blocked
18:59 metastasis but I was unhappy with those
19:03 drugs because of their associated
19:05 serious adverse events so my prison
19:08 looking at things is how do I help my
19:10 patients you know my training was in
19:12 oncology start off in bone marrow
19:13 transplants and when you add something
19:15 in to current standard of care you
19:18 usually add it in to chemotherapy some
19:20 sort of quite toxic treatment so when I
19:23 was doing the thought experiment of
19:25 adding in a small molecule inhibitor to
19:27 the standard of care chemotherapy where
19:30 the small molecule inhibitor had a lot
19:32 of
19:32 serious adverse events I was concerned
19:34 at how this might actually get into
19:36 clinical practice so as not a mentioned
19:40 I contacted cider Dean and asked if I
19:44 could test their antibody in our essays
19:47 and this was the first result where we
19:49 demonstrated that Pro and forty binds to
19:52 cancer ccr5 and it blocks this migration
19:55 of cancer cells
19:57 now when you if you're a an immune cell
20:01 and ccr5 is activated you start moving
20:05 the first thing you do is you turn on
20:07 calcium signaling it's a gas going into
20:09 the car and that's also true in the case
20:11 of a cancer cell expressing ccr5 so we
20:14 looked at cancer calcium signaling as a
20:16 initial surrogate endpoint and this is
20:20 calcium signaling here this is a little
20:22 blip and we can measure this calcium
20:24 signal but when we add Lauren ylim AB or
20:27 small molecule inhibitor we brought
20:28 block that calcium signal so basically
20:31 you block the gas going into the car and
20:35 it doesn't move so we Dex tested this in
20:38 mice that I'm going to show you two
20:40 types of cancer there are others first
20:43 the breast cancer story so these are
20:46 these are mice and these are the lungs
20:49 of mice that are filling up with
20:50 metastatic human breast cancer with time
20:53 so here we see four weeks and the mouse
20:55 lungs are now filled with this highly
20:59 metastatic breast cancer and these the
21:01 animals that have been true pre treated
21:03 with a ccr5 inhibitor and you can see
21:06 this quantitative here there's about a
21:07 95 percent reduction in metastatic
21:10 burden so these animals die and these
21:14 animals live and you can see the slope
21:17 of this curve so this is not putting on
21:19 you know a ten percent improvement in
21:21 survival this is a 95 percent reduction
21:24 in metastatic burden that ultimately
21:26 kills the mouse when we look in prostate
21:30 cancer we developed a new model of
21:33 metastatic prostate cancer part of the
21:35 reason we haven't really made a lot of
21:37 impact in treating and reducing the
21:40 mortality from prostate cancer
21:42 metastases we don't have great models to
21:44 test it in so we spent four or five
21:46 he is developing this model and this is
21:49 an immune competent mouse model so they
21:52 have a normal immune system and these
21:53 are the metastasis of the mice this
21:56 animals back is bent because it's broken
21:58 these are the metastases here in a spine
22:01 of the mice so highly metastatic
22:03 prostate cancer spreads to the bones and
22:06 brains of the mice kills the animals but
22:08 the animals that were pre treated with
22:09 the ccr5 and here but blocks the
22:11 metastases to the spine the spine is not
22:13 broken and these animals are able to run
22:16 around the cage they're going to fast
22:19 forward to human studies suffice it to
22:22 say that a lot of laboratories around
22:23 the world have moved into this field
22:26 ccr5 has become the new cancer kid on
22:28 the block a very hot topic in both in
22:33 the research area in laboratory but also
22:34 now in the clinic this is one example of
22:37 some studies that were conducted with
22:39 ccr5 inhibitors this was personally very
22:43 exciting to me this is a patient with
22:45 metastatic colon cancer and the way you
22:48 see the metastasis here where it lights
22:51 up red just like in the animal studies
22:52 these the metastasis is the lungs of in
22:55 this is the liver of the patient and
22:57 these are the metastases here so every
23:01 patient in this clinical study had
23:03 failed all possible available therapies
23:06 and their disease was progressing so
23:09 that was the entry criterion into this
23:11 study and this is the result after 60
23:13 days of treatment with a small molecule
23:15 inhibitor the metastases dramatically
23:18 reduced tumor volume now this is in of
23:22 itself a very exciting result but more
23:25 importantly when Duke Jagger and his
23:28 group colleagues who run who work at the
23:32 equivalent of the German Cancer
23:34 Institute the National Cancer Institute
23:36 in Germany when they looked at what's
23:39 happening in the metastases there was an
23:41 activation of the anti-tumor immune
23:43 response so in addition to the effect to
23:47 block the GPS or spread of the cancer it
23:50 was also activating the policeman the
23:52 anti-tumor immune response to go out and
23:54 kill the metastases so two independent
23:57 belts and braces two shots on goal
23:59 two different effects of the same ccr5
24:03 inhibitor so based on these and other
24:06 studies we have decided to move
24:09 initially into the year of triple
24:10 negative breast cancer in part because
24:13 of the current lack of options for these
24:16 women in part because the opportunity to
24:20 impact more than 95% of those patients
24:23 because they all express ccr5 the the
24:27 trial was approved by the FDA we have
24:29 moved forward therefore with us the
24:31 design is very straightforward
24:33 it's simply adding Pro 140 into the
24:36 standard of care carboplatin the
24:39 institutions that have signed up to be
24:41 participants in this clinical trial are
24:44 very high level Northwestern University
24:46 Laurie Cancer Center the Vanderbilt
24:48 Cancer Center Houston Methodist Thomas
24:51 Jefferson University Sidney Kimmel
24:52 Cancer Center and others because of the
24:55 enthusiasm because this type of
24:58 technology is without serious adverse
25:00 events and have shown dramatic
25:02 preclinical results this is an example
25:05 of colon cancer and again it's not a
25:08 mention there's about a 60 to 70 percent
25:09 reduction in the tumor volume of colon
25:12 cancer in mice I wondered spend just one
25:18 moment mentioning that we are involved
25:20 in non diluted funding efforts for the
25:24 company and that occurs now at the
25:26 highest level the strategy of the board
25:29 and senior management a unified ER and
25:31 the importance of forming strategic
25:33 alliances to identify the shortest path
25:36 to revenue in its company usually in
25:39 cancer the opportunities arise earlier
25:42 in that pipeline or usually successful
25:45 outcomes in Phase two the results that
25:48 lead to strategic alignments and and new
25:52 revenue coming into a company we've also
25:55 focused on licensing a technology for
25:58 prostate cancer prognostic testing in a
26:01 nutshell about a million men a year are
26:04 diagnosed having serial elevated PSA
26:07 sent to their doctor and the doctor says
26:10 when we need to
26:11 stick a needle into your prostate 12
26:13 times and we'll let you know what that
26:15 shows and after the prostate box about
26:18 250,000 minutes you will have been
26:21 diagnosed with prostate cancer the
26:23 question is is it a prostate cancer that
26:25 will kill you or will you die with it
26:28 from some other cause and so this test
26:30 distinguishes bad outcome from good
26:32 outcome prostate cancer there are
26:35 currently 3 incumbent tests in the
26:37 marketplace they itself from between
26:39 3500 and 5500 and this test has shown in
26:42 three independent clinical studies 5 to
26:45 10 you fought to be far superior to the
26:47 incumbent technology so we're pushing
26:49 hard to ensure we have a 510k with the
26:53 intent of licensing this technology so
26:57 I'd like to summarize where the company
27:00 is at right now it is an inflection
27:03 point in the in the company's history as
27:05 it pivots from HIV into cancer the
27:08 strategy around cancer is to initially
27:11 provide proof of principle with triple
27:13 negative breast cancer and then really
27:15 to look for a FDA approval for mechanism
27:20 so the intent is to move from triple
27:23 negative breast cancer ccr5 positive
27:25 triple negative breast cancer into ccr5
27:28 positive cancer and this is a strategy
27:30 that's proved successful for other
27:32 companies due to the FDA ruling and the
27:37 strong advocacy of the survivors cancer
27:41 survivors in this country and a very
27:42 wise move so again to recap the BL a
27:47 submission is moving forward under dr.
27:52 Paul Hassan's leadership and is moving
27:54 forward effectively with a revenue
27:57 potential that in the first year is
28:00 listed as being relatively modest market
28:02 penetration considering the size of this
28:05 market which is now you mentioned about
28:06 3 billion potential annual revenue there
28:11 is a Phase three pivotal trial which
28:14 intends to be initiated
28:16 we have FDA approval for this triple
28:19 negative breast cancer study and we
28:21 anticipate interim results within the
28:23 first half of this year
28:24 as we anticipate results upon initiating
28:28 or initiating the graft-versus-host
28:29 disease study we are seeking licensing
28:32 of this prognostic test upon completing
28:37 the 510k and there is the intent to move
28:40 into other cancers in 2019
28:43 starting with colon cancer based on the
28:46 successful outcome and the movement of
28:48 milk & Fire's into this space so the
28:52 company has come a long way in the last
28:53 three or four months spent pivoting from
28:55 historically and an HIV immune focused
29:00 company pivoting into cancer early
29:03 results are very exciting in that domain
29:06 and I would agree with nada this is a
29:09 company that has been doing on the HIV
29:12 side and has extraordinary upside
29:14 potential in the cancer domain so I'll
29:17 stop now answer any questions and thank
29:19 you for your time any questions
29:32 rich richard pesto
29:39 you have a medical practice how
29:42 important is the site to die in
29:44 relationship to you personally about 22
29:48 million shares yeah so most of my time
29:56 is spent on the road fundraising and
29:58 overseeing the expansion as clinical
30:00 medical medical officer into the cancer
30:02 space so I've been responsible for
30:05 ensuring that we move rapidly and
30:07 effectively into the the cancer space
30:10 overseen the construction of the IND for
30:14 triple negative breast cancer
30:15 identifying the relevant clinical sites
30:17 checking those sites out making sure
30:19 that this study is done effectively and
30:22 you know the responsibility here is to
30:25 not fail the technology the technology
30:26 is beautiful we just need to make sure
30:28 that we do things exactly the right way
30:31 and get the best people in the country
30:33 participating so the person who's doing
30:35 the administer chemistry for ccr5 is the
30:38 top guy in the country out of Minnesota
30:40 we got the top guy looking at
30:42 circulating tumor cells a father of CTCs
30:44 out of Northwestern and then we've got
30:46 four or five clinical sites that are
30:49 some of the best in the country so
30:50 that's how I'm spending you know 90% of
30:53 my waking time go ahead you got my join
31:03 me go ahead
31:12 would you sell that as an asset to
31:14 someone like a Gilead or the Orcas
31:16 license the technology because I mean a
31:19 chai company involved in HIV it won't be
31:21 a completely different kind of company
31:23 involving cancer right
31:25 no thanks for the question that question
31:27 is would we be selling HIV product by
31:30 itself perhaps and fund the rest of the
31:32 program we are in discussion with big
31:35 pharma but when you want to change Big
31:37 Pharma's a normal part of business that
31:41 they have conducted for many years
31:43 making great amount of money and helping
31:46 patients of the world which is a great
31:48 thing they have been doing now you're
31:50 going to go there and say ok we're going
31:51 to do it different so that's going to
31:53 take a little bit time to get that
31:56 mentality to accept something like this
31:59 with the result of our data convince
32:02 them we are in discussions so we don't
32:04 know anything or we that how they're
32:07 going to react but we are in discussion
32:09 there has been interest and we are
32:10 exploring exploring it and we are
32:13 definitely open to selling the HIV for
32:16 the right price according to our third
32:18 party buy of it that's the reason we did
32:20 that report to make sure we know what we
32:22 work for any other questions go ahead
32:30 the revenue for the price that we have
32:33 now which is $70,000 per year per
32:36 patients if you look at 49,000 patients
32:39 being impacted by that you're talking
32:41 about three over three billion dollars
32:43 worth of market there is a lot more
32:46 research needs to go to that but the
32:48 bottom line is we're talking about
32:50 patients who don't have other options
32:52 they have is they have got resistance
32:55 now there is another antibody that got
32:57 approved but that one is for patients
32:59 have to go to hospital or a care center
33:02 together IV every two weeks our
33:04 advantages so that might be they can't
33:06 self inject that's a great product also
33:08 but they had a 43% suppression rate at
33:12 the end of twenty four weeks
33:13 ours was 81% the revenue that we are
33:17 putting out here is based upon by Ovid
33:19 report which was a independent from us
33:21 they did a report we believe mono
33:23 therapy will also do a great job but
33:26 as you said maybe we should license the
33:28 HIV because we are now looking at
33:30 something much much bigger than HIV all
33:32 cancers that we could compare it but not
33:36 all cancers that you know all the cancer
33:38 that we are allowed to or we are put we
33:40 have potential for we're gonna explore
33:42 all of that so that's a huge market so
33:47 the revenue starts after we have our BL
33:50 a completely accepted by FDA we had put
33:54 a timeline of March which we have to now
33:56 based upon our discussion with FDA we're
33:59 going to have to put a press release out
34:00 saying when is our timelines when you
34:02 give your final DLA you got ten months
34:06 of standard waiting we have accelerated
34:08 up forward if that give us six months
34:10 then you're talking about so I'm
34:12 confidence in 2020 we'll have revenue
34:15 that's what I believe around one hundred
34:24 eighteen thousand and you have to go to
34:29 a professional institution either a
34:31 hospital to get intravenous injection
34:33 every two weeks so there's an additional
34:35 cost on top of that so I think the price
34:38 point of 70,000 may it be a tad
34:40 conservative and you know many of us
34:43 have thought pricing at 110,000 is
34:45 entirely reasonable in this particular
34:48 space I think it's important to
34:50 understand the company has been spending
34:52 a lot of its money on producing
34:55 commercial-grade antibody which is ready
34:57 for sale so a lot of companies don't
35:00 emphasize that but this has been going
35:03 on all the time behind the scenes if I
35:08 may add is if you get a breakthrough
35:10 designation for let's just say triple
35:12 negative breast cancer if there is not
35:14 going to give you a pull if you don't
35:16 have commercial product approval for
35:18 what because there you have to stick or
35:20 get your commercial product which would
35:21 take two years for the last two years we
35:24 didn't stop that so we spend a lot of
35:27 money and everybody is saying why are
35:28 you spending so much money they don't
35:30 realize we spend 190 million so far for
35:33 all of these things and usually takes
35:36 half a billion dollar to get a product
35:38 to the market so I think
35:40 it's a very satisfying for me to say
35:43 that we didn't use half a billion we use
35:45 this much and we're where we are and we
35:47 do have commercial products sitting in
35:49 the warehouse right now yes so you've
35:51 spent you know 190 million dollars and
35:54 you got 200 million of commercial great
35:56 anybody sitting in a warehouse you know
35:58 I think and you developed the technology
36:00 for free basically it's pretty
36:02 astonishing yeah sure the design of the
36:23 triple negative breast cancer study is
36:25 relatively straightforward there's a
36:27 dose escalation phase for 18 patients
36:30 with the intent we believe of confirming
36:33 that 700 milligrams is safe in this
36:35 patient population as you know there's
36:37 been some 660 patients treated to date
36:41 and with Lorana lab and at this stage
36:44 have been no serious adverse events but
36:46 the reason for doing this dose
36:48 escalation is we'd like to use the 7 or
36:50 milligram dose and the subsequent 30
36:53 patients will be treated with that 700
36:57 milligrams oh so if there are no issues
36:58 with that dose in this patient
37:00 population important to the study is we
37:02 do measure what's called circulating
37:04 tumor cells so although the primary
37:07 endpoints are the standard endpoints as
37:09 you see in cancer progression free
37:11 survival overall survival rate we're
37:15 also measuring a blood test so we take
37:18 blood from these patients 21 days after
37:20 we give them the Rana map and we measure
37:24 the circulating tumor cell number so
37:25 this is a secondary endpoint a surrogate
37:28 secondary endpoint and this information
37:30 will be provided to the FDA as an
37:33 earlier time point so our intent is to
37:35 use the circulating tumor cell data
37:37 share that with the FDA expeditiously in
37:40 terms of the graph versus oh sorry
37:43 in terms of the graft-versus-host
37:45 disease study which we intend to reopen
37:47 the plan here is to change the entry
37:50 criterion that said that's the only
37:52 significant
37:53 change in the way in which the study is
37:55 designed and the intent here is to
37:57 include only the low dose you know
38:00 radiation priming group of patients and
38:03 have a common conditioning regimen for
38:06 the patients before there was a lot of
38:08 different conditioning regimens and it's
38:10 very hard to see a difference when
38:12 everyone comes to you with a different
38:13 background treatment so my intent was to
38:16 meet with all of the thought leaders all
38:18 the principal investigators having met
38:20 with them all over the last couple of
38:22 months
38:22 get a consensus around what a common
38:25 conditioning regimen would be that and
38:27 the selection criterion has now been
38:29 modified so the intent would be to
38:32 reopen that study again this is a 14
38:35 week study in GVHD so we're not talking
38:38 about two years this is a 14 week study
38:41 and I think it's important to emphasize
38:43 in the cancer space the Barra set quite
38:47 quite a different level to to HIV 14
38:50 week study in GVHD
38:52 please
39:26 if I could go back to the hid if I
39:29 recall correctly when acutely I bought
39:31 pharmacy for the 11 billion evaluation
39:33 the pharmacy asset was a lot earlier in
39:37 the stage of the development and proved
39:39 and where pro 140 is I mean or said
39:42 another way for 140 is a lot farther
39:44 along almost your approval then where so
39:50 I'm gonna let dr. past and say that but
39:52 I can only say one comment about that
39:54 day
39:55 Gilead passed on that opportunity few
39:58 years ago for around four billion end up
40:01 paying 12 billion or something just a
40:04 little after that but do you have any
40:06 information so I think embedded in the
40:09 question is what has been interaction
40:12 with Gilead at this stage and what is
40:14 the level of understanding of what's
40:16 going on here and I think my impression
40:19 is that there's not been the level of
40:21 communication within the organization as
40:23 to and there's been some sort of
40:26 transparency as easy as it should have
40:27 been and we're working on that aspect of
40:30 communicating more clearly to the higher
40:31 levels of the organization now per
40:33 system best way to to state that I agree
40:45 100 percent agree with you that's a
40:47 great point
40:47 yeah any other questions
40:54 yeah please yes so the the study design
41:02 is a dose escalation for the first 18
41:05 patients three fifty five three five and
41:07 then a seven hundred milligram and if we
41:09 see no issues with dose related toxicity
41:12 which we don't anticipate then we'll use
41:14 the seven or milligrams we just wanted
41:16 to go slow do it safe do it right by the
41:19 patients we don't anticipate there are
41:21 going to be any adverse events related
41:24 to the dose escalation component study
41:26 but we thought it was better to go go
41:28 slow go safe and one thing I would like
41:31 to add to that is the first 18 patients
41:33 that we do those excavation we still
41:37 take in the CTC circulating tumor cell
41:39 all of these patients also so in the
41:42 event those first ten of those 18 or 15
41:45 come out to have the CTC that's reduced
41:47 drastically the first thing we're going
41:50 to do is to ask about breakthrough
41:51 designation when I get to Phase two
41:56 it stated the dose exclusion exactly
42:11 exactly yes I think not is pointing out
42:15 that there will be new information
42:17 coming out relatively soon in several
42:21 different high impact areas which we
42:24 think will be very helpful further
42:27 current investors and the current round
42:30 of investment
42:37 yeah rock-solid
42:39 yes thank you very much everybody up
42:46 [Applause]
Here is NobelCon15 transcript on January 28th
00:03 thank you everyone for being here for
00:05 Saturday and presentation excited on our
00:10 lead product is liran Lima Pro 1:40 we
00:16 are developing Lear on the map for HIV
00:18 and cancer I will be making
00:21 forward-looking statements
00:26 biotechs are usually when there have a
00:29 stock price below $1 they call them
00:33 high-risk high-reward I'm going to make
00:37 a case today that we are low-risk
00:39 high-reward
00:40 the reason for that is we had our
00:43 primary endpoint I mean it's all about
00:46 getting your phase 3 completed we
00:48 completed that and we have done much
00:51 more than that so I believe it's
00:53 low-risk high-reward we started
00:57 developing this product for HIV our
01:01 first phase 3 pivotal trial is a world's
01:05 first self injectable product for
01:08 patients who could die if they don't
01:12 have this product HIV does not kill
01:15 anymore there are products that will be
01:17 able to make this deadly disease a
01:20 chronic disease but not for this
01:23 population this population patients that
01:25 have three or four classes resistance
01:29 they have AIDS
01:30 so we're not talking about a population
01:33 that's just the normal population it's a
01:35 population that you are in great need of
01:38 this product so this is a first self
01:41 injectable antibody for that population
01:44 the unmet medical need population we
01:49 also have another phase three that one
01:52 is not a pivotal trial that one's going
01:55 to need a pivotal trial after it's
01:57 completed the reason that trial was
02:00 going on is because we have a lot of
02:01 interest on this product for mono
02:04 therapy Gilead and viv are working on
02:10 the next generation of products for HIV
02:12 they've developed two
02:16 two component product for HIV all the
02:22 HIV products are three component if they
02:25 don't have three component they're not a
02:27 regimen that can stop HIV from killing
02:31 we've developed a product with two
02:33 components they spent several hundred
02:36 millions of dollars this trial is a
02:39 single component one product
02:42 it's not even synthetic drug it's
02:44 humanized monoclonal antibody we have
02:49 patients who were taking four or five
02:51 pills a day three pills a day an exact
02:53 time they had to take it because if they
02:55 miss a dega resistance resistance is
02:57 dangerous in the world of HIV and they
02:59 have gone four years some of them four
03:02 and a half years without any standard
03:05 care pills just simple injectable sub-q
03:09 at home once a week 30 seconds and
03:12 they're done so that's our HIV story the
03:17 next one is graft-versus-host disease we
03:20 were surprised when Pfizer came back
03:22 came out and says our HIV product has
03:25 indication in GVHD leukemia patients who
03:28 need bone marrow transplant so we did in
03:30 vitro study ten thousand dollars cost
03:32 the study FDA gave us Phase two skipping
03:36 all the development that's how much FDA
03:40 thinks of this product that's what we
03:42 have fast track designation that's what
03:43 we got twenty eight million dollars
03:45 water grant from NIH at the early time
03:47 but this product was being developed
03:50 tnbc triple negative breast cancer now
03:54 waiting to cancer world-renowned
03:57 oncologists figured out that there's
03:58 another use for the mechanism of action
04:01 for HIV product that are ccr5
04:04 antagonists we're going to get to that
04:06 that's our very important study colon
04:10 cancer Phase two we want to be not in
04:12 Phase two we want to file an IND
04:13 initially drug application for FDA to
04:16 give us another Phase two for another
04:18 indication and prognostic tests we'll
04:21 talk about that we like to get approval
04:23 for that this year hopefully we're going
04:25 to talk to FDA all the studies have been
04:27 done so what's the mechanism of
04:31 this product that has so many potential
04:34 perhaps next Humira if you look at if
04:39 you look at the cell HIV doesn't kill
04:44 anybody if it doesn't intercellular you
04:49 get a flu you find if it doesn't enter
04:52 the cell our product stops the virus
04:54 from going into the cell before the
04:57 whole thing starts it stops it and
05:00 here's a magnified picture of the
05:04 membrane there's two receptor cd4 ccr5
05:08 dr. paul madden invented I mean
05:10 discovered that HIV has to interact with
05:13 this receptor and then this one to get
05:15 in there so he invented through one
05:18 fully round him a pro 140 he discovered
05:21 that dr. Richard pastel on the other
05:23 hand discovered that there is another
05:25 use for this and octopus sir will had
05:27 address you about the potential other
05:29 potential of this product so at the
05:33 early time when this product was being
05:36 developed to 12 years ago FDA gave it
05:41 fast track designation stating that
05:44 there are clear advantages of leer only
05:48 map where it says current standard of
05:50 care we have a letter from FDA says you
05:53 got fast track designation and these
05:55 were the reason they cited twenty eight
05:57 million dollars from NIH was given to
05:59 this product I get the last six million
06:02 dollars back to NIH because I thought
06:04 that this product has a lot more
06:06 potential than just going after
06:08 substance abuse population that was five
06:11 years ago today I'm proud to say that
06:14 that was a good path we took here's our
06:19 first combination therapy 52 patients
06:23 were there because this is unmet medical
06:25 need population primary endpoint hit
06:28 p-value point zero zero three eighty one
06:31 percent of the patients who never some
06:34 of them never could have suppressed
06:35 viral load suppressed viral load means
06:38 you don't chance meet HIV to somebody
06:42 else very crucial for other
06:44 not just for the patient alone 81% had
06:48 suppressed viral load we have letter
06:50 from a physician saying my patient for
06:52 27 years didn't have suppressed viral or
06:55 do not take this patient already pro 140
06:57 at the end of the study so we didn't
06:59 either had 45 percent for 48 weeks we
07:03 had eighty one percent I believe zoom at
07:06 last product got approved forty three
07:08 percent for 24 weeks we never had any
07:11 serious adverse event with this product
07:13 for the last 670 patient that is related
07:16 to pro 140 later on Lima we don't this
07:19 product is safe this product is really
07:23 stated about state about so 40 patients
07:27 from this population is still I went to
07:30 the extension we still have close to 30
07:33 patients in extension some are gone for
07:35 three years close to three years now
07:37 three years regulatory pathway we met
07:40 with FDA we are carefully crafting a
07:44 press release to come out about our
07:47 meeting with FDA just last December just
07:51 last month we we had a conference call
07:53 with FDA to fine-tune our BL a biologic
07:57 license application I'm very excited
07:59 about that and we will be looking at FDA
08:02 minutes to just make sure that we
08:04 reflect exactly what we got we are this
08:06 far away from approval so we want to
08:08 make sure that we indicate to everybody
08:11 what's happening these last few weeks or
08:14 months before we get to the submission
08:16 of B la mano therapy we also discussed
08:21 that with FDA we will be putting out
08:24 press release about that also our
08:26 responders rate in the past was said to
08:28 be 90% 700 milligrams we will be update
08:30 you get you everybody about that but we
08:33 have a path to approval now we got there
08:36 high responders and we set out so many
08:39 things to do
08:39 done every one of them and we're
08:42 successful in every one of them having
08:45 failed in combination therapy primary
08:47 endpoint haven't failed on finishing the
08:49 trial with a great result haven't failed
08:51 to get mono therapy to the finish line
08:52 we have a fail to find out other
08:55 indication for this product so
08:58 to that let's look at the market size
09:00 for combination therapy I'm gonna go
09:03 with this slide we had a hard time
09:05 pricing this product before we put lower
09:07 price here but then well as we are
09:09 talking right now with Big Pharma which
09:11 we said to everybody we're talking to
09:12 Big Pharma's we realize if we priced it
09:15 for HIV one price and for cancer and
09:18 other one is going to be disaster
09:19 getting this license for each indication
09:22 so what we did is we put a $70,000 price
09:25 the current product for HIV unmet
09:29 medical need is selling from 100 $18,000
09:32 per patient per year current antibody
09:35 for cancer is selling for $70,000 per
09:39 year per patient so we'll go with 70s
09:41 Devi that with all the indication that
09:43 we might have the market size for this
09:45 combination therapy is pretty
09:47 significant and for mono therapy is much
09:50 higher this is the report from
09:54 independent report by Ovid going to the
09:57 patient's doctors to payers and they
10:00 said that one of the things that they
10:01 said is 95% of HIV patients said they
10:04 would have no problem using this
10:06 injectable they're not going to worry
10:08 some big formal says hey they might not
10:10 take injectable big for most we said no
10:12 here it is 85% take it no problem from
10:16 mono therapy 95% for combination so that
10:20 concludes everything about HIV what we
10:23 were shocked when Pfizer comes back and
10:25 says this product has their product the
10:28 ccr5 antagonists which got approved
10:30 maroc has a blackbox warning has side
10:32 effect has to be taken by patients twice
10:35 a day pills this is not that so that
10:38 product is not comparable ours we did
10:42 GVHD we compared our self Tamara Brock
10:44 in in vitro study we had good results so
10:47 we went ahead and sent that results to
10:49 the FDA we got phase two when I asked
10:52 for orphan drug designation the FDA says
10:54 take two groups of 32 miles inject all
10:57 of them with human bone marrow if all of
11:01 them died then that means you know human
11:04 bone broke kills the mice but give half
11:06 of them near on the map if some of them
11:09 are stay alive
11:10 you got yourself orphan drug
11:11 nation 100% of the mice stayed alive a
11:15 hundred percent of the other mice died
11:17 because it's a hundred percent we did it
11:20 again and again and again and a result
11:23 same saying the mice that had no Lear on
11:27 the map their weight loss was drastic
11:29 night and day so we got off on drug
11:32 designation then that's when we got
11:35 shocked when we hear dr. Richard pastel
11:38 500 patients pay per published in
11:41 peer-reviewed journal I published one
11:43 paper I got my PhD in mechanical
11:44 engineering we did 500 so figure it out
11:48 he comes to us and says I discovered
11:52 something I discovered and I published
11:55 it that the metastasis of cancer that is
11:57 responsible for killing mankind can be
12:00 stopped by your product now when you
12:04 find something like he did you don't you
12:07 can't do anything with that you gotta
12:09 have a product that does that so Pfizer
12:11 and marek approached him they did this
12:14 study
12:14 he holds the patent now we hold it
12:16 because we acquired his company but then
12:19 he didn't like Pfizer and where he come
12:21 to us he said yours doesn't have any
12:23 serious adverse event or toxicity that
12:27 is comparable to Maryborough it's hardly
12:29 any toxicity or side effect so I wanted
12:31 I want your product we said we don't
12:33 have any money he said we don't want
12:36 money we want shares of your stock
12:39 that's a valuable valuable commodity and
12:42 we did the deal so sure so we have the
12:46 brain trust in our company now he talks
12:48 about his discovery that needs our
12:52 product so we have patented everything
12:54 and it's been almost honor for me to
12:58 work with this gentleman and I'm very
13:00 pleased to introduce him so he can
13:02 explain everything doctor person well
13:07 good afternoon everybody can you hear me
13:09 up the back I'm very pleased to be here
13:12 today and to be involved with cider dine
13:15 at this pivotal moment in their history
13:17 I'm relatively new to the company
13:19 compared to most everybody in this room
13:21 we formally sold our company didn't
13:25 member 2018 and a lot has happened the
13:28 last couple of months I thought I'd
13:30 share with you a couple of insights
13:32 related to how and why the company has
13:36 pivoted from HIV into cancer in a
13:40 nutshell nada shared with you that
13:42 sighted on is a publicly traded company
13:45 that is on the OTC as a market cap of
13:48 around hundred fifty five million that
13:50 has successfully completed a phase three
13:52 study for HIV having met all its primary
13:55 endpoints that's currently conducting
13:57 its PLA and is a highly de-risked
13:59 company in that context my laboratory
14:03 about seven or eight years ago had been
14:07 investigating the mechanisms by which a
14:10 cancer cell metastasizes and at that
14:14 time it really wasn't understood exactly
14:16 how that happens and it's the spread of
14:19 cancer that kills people now to mention
14:22 to you today that there's a receptor
14:24 called ccr5 which is essential for entry
14:27 of HIV into the t-cell that ain't what
14:31 it usually does okay what what CC r45
14:35 normally does on it on a t-cell is to
14:37 direct its movement so when a t-cell
14:41 activates ccr5 or its ligand it moves so
14:45 one of the normal functions of immune
14:46 cells they're policemen of the body
14:49 tracking down infections and
14:51 inflammation and the cell moves because
14:54 of the ccr5 pressed on cell surface now
14:59 we found that surprisingly when we use
15:03 an artificial intelligence approach that
15:05 cancer cells turn on that same receptor
15:08 and when a cancer cell does that it
15:10 starts moving so we showed that this
15:14 receptor normally expressed just on T
15:16 cells promoting migration to the bones
15:19 and brains the other place where immune
15:22 cells go does the same thing for a
15:24 cancer cell so the ccr5 is necessary and
15:28 sufficient for the movement of cancer
15:29 cells to the bone to the brain to the
15:32 lungs and other tissues
15:34 now note i had mentioned what we had
15:38 which was to study a variety of
15:40 different cancers and I'm going to show
15:42 you some primary data but just to
15:45 preempt it we looked at 2200 patients
15:48 with breast cancer we look at every gene
15:51 in their cancer and we found that about
15:54 50% of breast cancers overexpress ccr5
15:58 50% so the previous blockbuster which
16:02 was Herceptin targets about 12 to 15% of
16:06 human breast cancers but unlike
16:08 Herceptin ccr5 is turned on in other
16:11 cancers it's turned on about 50% of
16:14 prostate cancers pancreatic cancer colon
16:17 cancer variety of different types of
16:19 metastases I was particularly struck by
16:23 colon cancer both my parents died of
16:27 metastatic colon cancer and you know my
16:31 father was a cancer surgeon he was here
16:34 at SLU who's at sloan-kettering and
16:36 ultimately moved to Australia to Perth
16:39 big guy six foot two high jump champion
16:41 sprint champion and when he had
16:44 metastatic colon cancer he he couldn't
16:46 stand up to take a pee so this is a
16:48 disease that brings a strongest man a
16:50 woman to their knees so when we found
16:52 that there was a receptor which was
16:55 targetable that was driving that
16:57 metastatic process I was very excited at
17:01 a very deep level about the potential of
17:03 shifting this game in in the cancer
17:05 metastasis field thank you
17:14 excellent
17:18 so this is some of the the primary data
17:21 and this is a study with 2200 patients
17:27 so patient one two three four to 2200
17:30 and this is every gene in their cancer
17:33 and this arrow means this is ccr5 and so
17:37 ccr5 is turned on where it's red so all
17:40 these patients have ccr5 turned on the
17:44 cancers to these other patients but I
17:46 was very focused on this group of
17:47 patients because triple negative breast
17:50 cancer is a terrible terrible disease
17:52 now I've been looking after patients for
17:54 nine thirty years and triple negative
17:56 metastatic triple negative breast cancer
17:58 typically kills a woman within nine to
18:01 ten months at the time they appear in
18:03 your office typically attacks Eskenazi
18:06 Jewish women women of that descent
18:08 African American women and we currently
18:10 don't have any targeted therapy the
18:15 standard of care is chemotherapy and
18:17 surgery so identifying this as a
18:20 potential target ccr5 and all these
18:23 women was very very exciting and this is
18:26 I hope you can see this these are the
18:28 breast cancer cells here and this is
18:30 their their metastasizing in this case
18:32 they're invading through Maitre gel and
18:34 this is at their journey and here you
18:37 can see we had Lauren Elam AB Pro 140
18:39 when we used this small molecule on here
18:42 but we dramatically cut that invasion
18:45 and Stokes dependent we upped the dose
18:46 we block the the invasion and metastasis
18:49 now nada had intended to mean that when
18:54 I had used the Merck and Pfizer drugs I
18:57 had demonstrated that they blocked
18:59 metastasis but I was unhappy with those
19:03 drugs because of their associated
19:05 serious adverse events so my prison
19:08 looking at things is how do I help my
19:10 patients you know my training was in
19:12 oncology start off in bone marrow
19:13 transplants and when you add something
19:15 in to current standard of care you
19:18 usually add it in to chemotherapy some
19:20 sort of quite toxic treatment so when I
19:23 was doing the thought experiment of
19:25 adding in a small molecule inhibitor to
19:27 the standard of care chemotherapy where
19:30 the small molecule inhibitor had a lot
19:32 of
19:32 serious adverse events I was concerned
19:34 at how this might actually get into
19:36 clinical practice so as not a mentioned
19:40 I contacted cider Dean and asked if I
19:44 could test their antibody in our essays
19:47 and this was the first result where we
19:49 demonstrated that Pro and forty binds to
19:52 cancer ccr5 and it blocks this migration
19:55 of cancer cells
19:57 now when you if you're a an immune cell
20:01 and ccr5 is activated you start moving
20:05 the first thing you do is you turn on
20:07 calcium signaling it's a gas going into
20:09 the car and that's also true in the case
20:11 of a cancer cell expressing ccr5 so we
20:14 looked at cancer calcium signaling as a
20:16 initial surrogate endpoint and this is
20:20 calcium signaling here this is a little
20:22 blip and we can measure this calcium
20:24 signal but when we add Lauren ylim AB or
20:27 small molecule inhibitor we brought
20:28 block that calcium signal so basically
20:31 you block the gas going into the car and
20:35 it doesn't move so we Dex tested this in
20:38 mice that I'm going to show you two
20:40 types of cancer there are others first
20:43 the breast cancer story so these are
20:46 these are mice and these are the lungs
20:49 of mice that are filling up with
20:50 metastatic human breast cancer with time
20:53 so here we see four weeks and the mouse
20:55 lungs are now filled with this highly
20:59 metastatic breast cancer and these the
21:01 animals that have been true pre treated
21:03 with a ccr5 inhibitor and you can see
21:06 this quantitative here there's about a
21:07 95 percent reduction in metastatic
21:10 burden so these animals die and these
21:14 animals live and you can see the slope
21:17 of this curve so this is not putting on
21:19 you know a ten percent improvement in
21:21 survival this is a 95 percent reduction
21:24 in metastatic burden that ultimately
21:26 kills the mouse when we look in prostate
21:30 cancer we developed a new model of
21:33 metastatic prostate cancer part of the
21:35 reason we haven't really made a lot of
21:37 impact in treating and reducing the
21:40 mortality from prostate cancer
21:42 metastases we don't have great models to
21:44 test it in so we spent four or five
21:46 he is developing this model and this is
21:49 an immune competent mouse model so they
21:52 have a normal immune system and these
21:53 are the metastasis of the mice this
21:56 animals back is bent because it's broken
21:58 these are the metastases here in a spine
22:01 of the mice so highly metastatic
22:03 prostate cancer spreads to the bones and
22:06 brains of the mice kills the animals but
22:08 the animals that were pre treated with
22:09 the ccr5 and here but blocks the
22:11 metastases to the spine the spine is not
22:13 broken and these animals are able to run
22:16 around the cage they're going to fast
22:19 forward to human studies suffice it to
22:22 say that a lot of laboratories around
22:23 the world have moved into this field
22:26 ccr5 has become the new cancer kid on
22:28 the block a very hot topic in both in
22:33 the research area in laboratory but also
22:34 now in the clinic this is one example of
22:37 some studies that were conducted with
22:39 ccr5 inhibitors this was personally very
22:43 exciting to me this is a patient with
22:45 metastatic colon cancer and the way you
22:48 see the metastasis here where it lights
22:51 up red just like in the animal studies
22:52 these the metastasis is the lungs of in
22:55 this is the liver of the patient and
22:57 these are the metastases here so every
23:01 patient in this clinical study had
23:03 failed all possible available therapies
23:06 and their disease was progressing so
23:09 that was the entry criterion into this
23:11 study and this is the result after 60
23:13 days of treatment with a small molecule
23:15 inhibitor the metastases dramatically
23:18 reduced tumor volume now this is in of
23:22 itself a very exciting result but more
23:25 importantly when Duke Jagger and his
23:28 group colleagues who run who work at the
23:32 equivalent of the German Cancer
23:34 Institute the National Cancer Institute
23:36 in Germany when they looked at what's
23:39 happening in the metastases there was an
23:41 activation of the anti-tumor immune
23:43 response so in addition to the effect to
23:47 block the GPS or spread of the cancer it
23:50 was also activating the policeman the
23:52 anti-tumor immune response to go out and
23:54 kill the metastases so two independent
23:57 belts and braces two shots on goal
23:59 two different effects of the same ccr5
24:03 inhibitor so based on these and other
24:06 studies we have decided to move
24:09 initially into the year of triple
24:10 negative breast cancer in part because
24:13 of the current lack of options for these
24:16 women in part because the opportunity to
24:20 impact more than 95% of those patients
24:23 because they all express ccr5 the the
24:27 trial was approved by the FDA we have
24:29 moved forward therefore with us the
24:31 design is very straightforward
24:33 it's simply adding Pro 140 into the
24:36 standard of care carboplatin the
24:39 institutions that have signed up to be
24:41 participants in this clinical trial are
24:44 very high level Northwestern University
24:46 Laurie Cancer Center the Vanderbilt
24:48 Cancer Center Houston Methodist Thomas
24:51 Jefferson University Sidney Kimmel
24:52 Cancer Center and others because of the
24:55 enthusiasm because this type of
24:58 technology is without serious adverse
25:00 events and have shown dramatic
25:02 preclinical results this is an example
25:05 of colon cancer and again it's not a
25:08 mention there's about a 60 to 70 percent
25:09 reduction in the tumor volume of colon
25:12 cancer in mice I wondered spend just one
25:18 moment mentioning that we are involved
25:20 in non diluted funding efforts for the
25:24 company and that occurs now at the
25:26 highest level the strategy of the board
25:29 and senior management a unified ER and
25:31 the importance of forming strategic
25:33 alliances to identify the shortest path
25:36 to revenue in its company usually in
25:39 cancer the opportunities arise earlier
25:42 in that pipeline or usually successful
25:45 outcomes in Phase two the results that
25:48 lead to strategic alignments and and new
25:52 revenue coming into a company we've also
25:55 focused on licensing a technology for
25:58 prostate cancer prognostic testing in a
26:01 nutshell about a million men a year are
26:04 diagnosed having serial elevated PSA
26:07 sent to their doctor and the doctor says
26:10 when we need to
26:11 stick a needle into your prostate 12
26:13 times and we'll let you know what that
26:15 shows and after the prostate box about
26:18 250,000 minutes you will have been
26:21 diagnosed with prostate cancer the
26:23 question is is it a prostate cancer that
26:25 will kill you or will you die with it
26:28 from some other cause and so this test
26:30 distinguishes bad outcome from good
26:32 outcome prostate cancer there are
26:35 currently 3 incumbent tests in the
26:37 marketplace they itself from between
26:39 3500 and 5500 and this test has shown in
26:42 three independent clinical studies 5 to
26:45 10 you fought to be far superior to the
26:47 incumbent technology so we're pushing
26:49 hard to ensure we have a 510k with the
26:53 intent of licensing this technology so
26:57 I'd like to summarize where the company
27:00 is at right now it is an inflection
27:03 point in the in the company's history as
27:05 it pivots from HIV into cancer the
27:08 strategy around cancer is to initially
27:11 provide proof of principle with triple
27:13 negative breast cancer and then really
27:15 to look for a FDA approval for mechanism
27:20 so the intent is to move from triple
27:23 negative breast cancer ccr5 positive
27:25 triple negative breast cancer into ccr5
27:28 positive cancer and this is a strategy
27:30 that's proved successful for other
27:32 companies due to the FDA ruling and the
27:37 strong advocacy of the survivors cancer
27:41 survivors in this country and a very
27:42 wise move so again to recap the BL a
27:47 submission is moving forward under dr.
27:52 Paul Hassan's leadership and is moving
27:54 forward effectively with a revenue
27:57 potential that in the first year is
28:00 listed as being relatively modest market
28:02 penetration considering the size of this
28:05 market which is now you mentioned about
28:06 3 billion potential annual revenue there
28:11 is a Phase three pivotal trial which
28:14 intends to be initiated
28:16 we have FDA approval for this triple
28:19 negative breast cancer study and we
28:21 anticipate interim results within the
28:23 first half of this year
28:24 as we anticipate results upon initiating
28:28 or initiating the graft-versus-host
28:29 disease study we are seeking licensing
28:32 of this prognostic test upon completing
28:37 the 510k and there is the intent to move
28:40 into other cancers in 2019
28:43 starting with colon cancer based on the
28:46 successful outcome and the movement of
28:48 milk & Fire's into this space so the
28:52 company has come a long way in the last
28:53 three or four months spent pivoting from
28:55 historically and an HIV immune focused
29:00 company pivoting into cancer early
29:03 results are very exciting in that domain
29:06 and I would agree with nada this is a
29:09 company that has been doing on the HIV
29:12 side and has extraordinary upside
29:14 potential in the cancer domain so I'll
29:17 stop now answer any questions and thank
29:19 you for your time any questions
29:32 rich richard pesto
29:39 you have a medical practice how
29:42 important is the site to die in
29:44 relationship to you personally about 22
29:48 million shares yeah so most of my time
29:56 is spent on the road fundraising and
29:58 overseeing the expansion as clinical
30:00 medical medical officer into the cancer
30:02 space so I've been responsible for
30:05 ensuring that we move rapidly and
30:07 effectively into the the cancer space
30:10 overseen the construction of the IND for
30:14 triple negative breast cancer
30:15 identifying the relevant clinical sites
30:17 checking those sites out making sure
30:19 that this study is done effectively and
30:22 you know the responsibility here is to
30:25 not fail the technology the technology
30:26 is beautiful we just need to make sure
30:28 that we do things exactly the right way
30:31 and get the best people in the country
30:33 participating so the person who's doing
30:35 the administer chemistry for ccr5 is the
30:38 top guy in the country out of Minnesota
30:40 we got the top guy looking at
30:42 circulating tumor cells a father of CTCs
30:44 out of Northwestern and then we've got
30:46 four or five clinical sites that are
30:49 some of the best in the country so
30:50 that's how I'm spending you know 90% of
30:53 my waking time go ahead you got my join
31:03 me go ahead
31:12 would you sell that as an asset to
31:14 someone like a Gilead or the Orcas
31:16 license the technology because I mean a
31:19 chai company involved in HIV it won't be
31:21 a completely different kind of company
31:23 involving cancer right
31:25 no thanks for the question that question
31:27 is would we be selling HIV product by
31:30 itself perhaps and fund the rest of the
31:32 program we are in discussion with big
31:35 pharma but when you want to change Big
31:37 Pharma's a normal part of business that
31:41 they have conducted for many years
31:43 making great amount of money and helping
31:46 patients of the world which is a great
31:48 thing they have been doing now you're
31:50 going to go there and say ok we're going
31:51 to do it different so that's going to
31:53 take a little bit time to get that
31:56 mentality to accept something like this
31:59 with the result of our data convince
32:02 them we are in discussions so we don't
32:04 know anything or we that how they're
32:07 going to react but we are in discussion
32:09 there has been interest and we are
32:10 exploring exploring it and we are
32:13 definitely open to selling the HIV for
32:16 the right price according to our third
32:18 party buy of it that's the reason we did
32:20 that report to make sure we know what we
32:22 work for any other questions go ahead
32:30 the revenue for the price that we have
32:33 now which is $70,000 per year per
32:36 patients if you look at 49,000 patients
32:39 being impacted by that you're talking
32:41 about three over three billion dollars
32:43 worth of market there is a lot more
32:46 research needs to go to that but the
32:48 bottom line is we're talking about
32:50 patients who don't have other options
32:52 they have is they have got resistance
32:55 now there is another antibody that got
32:57 approved but that one is for patients
32:59 have to go to hospital or a care center
33:02 together IV every two weeks our
33:04 advantages so that might be they can't
33:06 self inject that's a great product also
33:08 but they had a 43% suppression rate at
33:12 the end of twenty four weeks
33:13 ours was 81% the revenue that we are
33:17 putting out here is based upon by Ovid
33:19 report which was a independent from us
33:21 they did a report we believe mono
33:23 therapy will also do a great job but
33:26 as you said maybe we should license the
33:28 HIV because we are now looking at
33:30 something much much bigger than HIV all
33:32 cancers that we could compare it but not
33:36 all cancers that you know all the cancer
33:38 that we are allowed to or we are put we
33:40 have potential for we're gonna explore
33:42 all of that so that's a huge market so
33:47 the revenue starts after we have our BL
33:50 a completely accepted by FDA we had put
33:54 a timeline of March which we have to now
33:56 based upon our discussion with FDA we're
33:59 going to have to put a press release out
34:00 saying when is our timelines when you
34:02 give your final DLA you got ten months
34:06 of standard waiting we have accelerated
34:08 up forward if that give us six months
34:10 then you're talking about so I'm
34:12 confidence in 2020 we'll have revenue
34:15 that's what I believe around one hundred
34:24 eighteen thousand and you have to go to
34:29 a professional institution either a
34:31 hospital to get intravenous injection
34:33 every two weeks so there's an additional
34:35 cost on top of that so I think the price
34:38 point of 70,000 may it be a tad
34:40 conservative and you know many of us
34:43 have thought pricing at 110,000 is
34:45 entirely reasonable in this particular
34:48 space I think it's important to
34:50 understand the company has been spending
34:52 a lot of its money on producing
34:55 commercial-grade antibody which is ready
34:57 for sale so a lot of companies don't
35:00 emphasize that but this has been going
35:03 on all the time behind the scenes if I
35:08 may add is if you get a breakthrough
35:10 designation for let's just say triple
35:12 negative breast cancer if there is not
35:14 going to give you a pull if you don't
35:16 have commercial product approval for
35:18 what because there you have to stick or
35:20 get your commercial product which would
35:21 take two years for the last two years we
35:24 didn't stop that so we spend a lot of
35:27 money and everybody is saying why are
35:28 you spending so much money they don't
35:30 realize we spend 190 million so far for
35:33 all of these things and usually takes
35:36 half a billion dollar to get a product
35:38 to the market so I think
35:40 it's a very satisfying for me to say
35:43 that we didn't use half a billion we use
35:45 this much and we're where we are and we
35:47 do have commercial products sitting in
35:49 the warehouse right now yes so you've
35:51 spent you know 190 million dollars and
35:54 you got 200 million of commercial great
35:56 anybody sitting in a warehouse you know
35:58 I think and you developed the technology
36:00 for free basically it's pretty
36:02 astonishing yeah sure the design of the
36:23 triple negative breast cancer study is
36:25 relatively straightforward there's a
36:27 dose escalation phase for 18 patients
36:30 with the intent we believe of confirming
36:33 that 700 milligrams is safe in this
36:35 patient population as you know there's
36:37 been some 660 patients treated to date
36:41 and with Lorana lab and at this stage
36:44 have been no serious adverse events but
36:46 the reason for doing this dose
36:48 escalation is we'd like to use the 7 or
36:50 milligram dose and the subsequent 30
36:53 patients will be treated with that 700
36:57 milligrams oh so if there are no issues
36:58 with that dose in this patient
37:00 population important to the study is we
37:02 do measure what's called circulating
37:04 tumor cells so although the primary
37:07 endpoints are the standard endpoints as
37:09 you see in cancer progression free
37:11 survival overall survival rate we're
37:15 also measuring a blood test so we take
37:18 blood from these patients 21 days after
37:20 we give them the Rana map and we measure
37:24 the circulating tumor cell number so
37:25 this is a secondary endpoint a surrogate
37:28 secondary endpoint and this information
37:30 will be provided to the FDA as an
37:33 earlier time point so our intent is to
37:35 use the circulating tumor cell data
37:37 share that with the FDA expeditiously in
37:40 terms of the graph versus oh sorry
37:43 in terms of the graft-versus-host
37:45 disease study which we intend to reopen
37:47 the plan here is to change the entry
37:50 criterion that said that's the only
37:52 significant
37:53 change in the way in which the study is
37:55 designed and the intent here is to
37:57 include only the low dose you know
38:00 radiation priming group of patients and
38:03 have a common conditioning regimen for
38:06 the patients before there was a lot of
38:08 different conditioning regimens and it's
38:10 very hard to see a difference when
38:12 everyone comes to you with a different
38:13 background treatment so my intent was to
38:16 meet with all of the thought leaders all
38:18 the principal investigators having met
38:20 with them all over the last couple of
38:22 months
38:22 get a consensus around what a common
38:25 conditioning regimen would be that and
38:27 the selection criterion has now been
38:29 modified so the intent would be to
38:32 reopen that study again this is a 14
38:35 week study in GVHD so we're not talking
38:38 about two years this is a 14 week study
38:41 and I think it's important to emphasize
38:43 in the cancer space the Barra set quite
38:47 quite a different level to to HIV 14
38:50 week study in GVHD
38:52 please
39:26 if I could go back to the hid if I
39:29 recall correctly when acutely I bought
39:31 pharmacy for the 11 billion evaluation
39:33 the pharmacy asset was a lot earlier in
39:37 the stage of the development and proved
39:39 and where pro 140 is I mean or said
39:42 another way for 140 is a lot farther
39:44 along almost your approval then where so
39:50 I'm gonna let dr. past and say that but
39:52 I can only say one comment about that
39:54 day
39:55 Gilead passed on that opportunity few
39:58 years ago for around four billion end up
40:01 paying 12 billion or something just a
40:04 little after that but do you have any
40:06 information so I think embedded in the
40:09 question is what has been interaction
40:12 with Gilead at this stage and what is
40:14 the level of understanding of what's
40:16 going on here and I think my impression
40:19 is that there's not been the level of
40:21 communication within the organization as
40:23 to and there's been some sort of
40:26 transparency as easy as it should have
40:27 been and we're working on that aspect of
40:30 communicating more clearly to the higher
40:31 levels of the organization now per
40:33 system best way to to state that I agree
40:45 100 percent agree with you that's a
40:47 great point
40:47 yeah any other questions
40:54 yeah please yes so the the study design
41:02 is a dose escalation for the first 18
41:05 patients three fifty five three five and
41:07 then a seven hundred milligram and if we
41:09 see no issues with dose related toxicity
41:12 which we don't anticipate then we'll use
41:14 the seven or milligrams we just wanted
41:16 to go slow do it safe do it right by the
41:19 patients we don't anticipate there are
41:21 going to be any adverse events related
41:24 to the dose escalation component study
41:26 but we thought it was better to go go
41:28 slow go safe and one thing I would like
41:31 to add to that is the first 18 patients
41:33 that we do those excavation we still
41:37 take in the CTC circulating tumor cell
41:39 all of these patients also so in the
41:42 event those first ten of those 18 or 15
41:45 come out to have the CTC that's reduced
41:47 drastically the first thing we're going
41:50 to do is to ask about breakthrough
41:51 designation when I get to Phase two
41:56 it stated the dose exclusion exactly
42:11 exactly yes I think not is pointing out
42:15 that there will be new information
42:17 coming out relatively soon in several
42:21 different high impact areas which we
42:24 think will be very helpful further
42:27 current investors and the current round
42:30 of investment
42:37 yeah rock-solid
42:39 yes thank you very much everybody up
42:46 [Applause]
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