Patterson:
32:30 thank you Nader it's
32:38 certainly a pleasure to be here talking
32:40 about one of my favorite subjects I
32:43 think it was a face that I met Nader
32:46 because I've spent 22 years working on
32:48 ccr5 first 15 in HIV funded by the
32:54 National Institutes of Health the last
32:56 five in the immuno oncology space
32:58 through my company incellDX the
33:02 important point about
33:03 ccr5 you see a lot of different in the
33:05 patience here you might say how can it
33:07 be effective against all of these
33:09 different indications well the fact is
33:12 ccr5 inhibitor Pro 140 it's like the
33:16 quarterback of the immune system so if
33:19 you look at any of those indications all
33:21 of them are driven by immune
33:23 responsiveness or a lack of immune
33:26 responsiveness and ccr5 is critical in
33:29 both of those contexts in terms of our
33:33 deal that we signed we indeed have
33:35 already ordered from CytoDyn our first
33:39 lot of pro 140 label with a fluorescent
33:43 dye so that we can sting tissues and
33:46 cells and say which cancer cells and the
33:49 immune cells associated with it and
33:51 which cells that HIV infects are
33:54 actually occupied by Pro 140 we actually
33:58 have the ideal tool to go to the FDA and
34:00 say listen this drug is working and an
34:03 irrespective of the viral load we know
34:06 this drug is working some of the things
34:08 that we're seeing on the ongoing HIV
34:11 trials are fascinating because Pro 140
34:15 acts on the cells that HIV infects and
34:18 protects them from being infected the
34:22 hallmark of HIV is the destruction of
34:24 the immune system as we all know and
34:26 AIDS right if you preserve the immune
34:30 system you're fine you have a competent
34:34 immune system that's what pro 140 does
34:36 it doesn't go in and inhibit the virus
34:40 like some of these other drugs do which
34:43 happen to be a lot more toxic than ccr5
34:46 but it blocks additional cells from
34:49 being infected which is really the
34:51 hallmark that's the goal of what
34:53 everybody should be looking for a good
34:55 analogy is I relate to you trying to
34:57 start a fire on your grill and you have
35:00 no charcoal but you have lighter fluid
35:02 so sometimes the lighter fluid will
35:05 light which I relate to an increase in
35:07 viral load but there's nothing to
35:10 propagate the fire so that you can cook
35:13 your hamburgers
35:13 right leronlimab
35:16 blocks the key cells that propagate
35:19 infection you need to prolonged
35:21 increases of viral load that's the
35:24 message that has to go to the FDA that
35:26 this drug is completely occupying the
35:29 receptors that it needs to occupy and
35:31 it's blocking virus from binding to
35:33 uninfected cells and preserving the
35:36 immune system that's where we all want
35:39 to be and in cancer ccr5 has been around
35:43 for a long time and it's not about ccr5
35:46 on the tumor
35:47 it's about ccr5 on certain immune cells
35:51 that that control the tumor okay so
35:54 there's two eight billion dollar-a-year
35:56 drugs called opdivo and keytruda
36:00 made by Merck and BMS that bring back
36:03 your own immune system to fight off the
36:05 tumor but you know what happens after
36:08 three to six months they stopped working
36:10 why do they stop working well this whole
36:13 new wave of cells comes in to shut that
36:17 immune response off that's part of the
36:19 elegance of our body in controlling you
36:23 know a immune response gone awry right
36:26 but in cancer we want the immune
36:28 response to go awry right those immune
36:32 cells called T reg cells that come in
36:34 and supposedly shut off the light switch
36:37 that opdivo and keytruda have turned back
36:40 on Express ccr5 so if we get pro 140 it
36:45 can block those cells from coming in and
36:48 shutting off the immune response that
36:50 you just spent two hundred thousand
36:52 dollars a year to bring back in the
36:54 patient it's a tremendous opportunity
36:56 this is a immuno oncology drug it is it
37:01 always has been and you know it hasn't
37:04 come to the forefront until just
37:06 recently now that we have more
37:08 information on how this immune response
37:11 against tumors is is regulated the other
37:14 thing that pro 140 does is it
37:16 reprogrammed
37:17 a cell called a macrophage think of
37:20 pac-man that little guy that goes around
37:22 and gobbles up little things on the
37:24 computer game
37:25 well macrophages come and gobble up
37:28 tumor cells normally right but when
37:31 they're when they're blocked by CCL 5
37:34 which is a protein made by t-cells they
37:38 don't go and gobble up the tumor cells
37:39 when you block with pro 140 those
37:43 macrophages are now active against the
37:45 tumor again so this is extremely
37:49 exciting immuno Oncology drug and you
37:53 know what I think the field is just
37:54 starting to realize it it's the
37:56 quarterback of cells moving in the body
37:59 to where they need to be and prolong for
38:02 taking control of that and now we have a
38:05 diagnostic that says this drug is going
38:07 to bind exactly in the past we've been
38:11 looking at ccr5 expression with antibody
38:13 bodies made by Dickinson and
38:15 other companies the problem is that
38:18 doesn't bind to the exact site that Pro
38:20 140 does so what we did in our deal is
38:23 we made sure that when we're doing
38:25 Diagnostics to see if there's a
38:27 candidate for pro 140 we're going to use
38:30 the actual drug as a diagnostic it's
38:34 elegant it's extremely elegant and it's
38:37 going to be much more specific and
38:39 accurate in defining the patients that
38:41 are going to respond and at the end of
38:43 the day we're all going to benefit from
38:45 that so I can't tell you how excited I
38:48 am about this and when you look at these
38:50 boards and all the different indications
38:51 it's easy to say well we're all over
38:53 the place in reality we're not what
38:56 we're just doing is taking advantage of
38:58 all the different disease states that
39:00 ccr5 is active in and this drug has
39:04 applications for all of those yet we
39:07 need to focus on the ones that are at
39:09 hand and get the HIV applications
39:12 approved but after that the pipeline
39:15 after that they'll just keep feeding
39:17 keep feeding the utility of pro 140 is
39:21 extremely excited really really exciting
39:25 both for the emulation standpoint and a
39:28 viral logic standpoint and again
39:30 for my work at Northwestern first and
39:33 then at Stanford this is what I spent my
39:35 life doing and finally this is coming to
39:38 the forefront so and I'm happy to answer
39:40 any questions any time show you any data
39:44 that we have internally that may not be
39:46 out to the masses or out to the FDA yet
39:48 because it is really really exciting
39:51 when I'm looking at this data coming off
39:53 our machines every single day there's
39:56 not a single day where I can't wait to
39:58 get into work and see that so we
40:09 definitely answer any question
32:30 thank you Nader it's
32:38 certainly a pleasure to be here talking
32:40 about one of my favorite subjects I
32:43 think it was a face that I met Nader
32:46 because I've spent 22 years working on
32:48 ccr5 first 15 in HIV funded by the
32:54 National Institutes of Health the last
32:56 five in the immuno oncology space
32:58 through my company incellDX the
33:02 important point about
33:03 ccr5 you see a lot of different in the
33:05 patience here you might say how can it
33:07 be effective against all of these
33:09 different indications well the fact is
33:12 ccr5 inhibitor Pro 140 it's like the
33:16 quarterback of the immune system so if
33:19 you look at any of those indications all
33:21 of them are driven by immune
33:23 responsiveness or a lack of immune
33:26 responsiveness and ccr5 is critical in
33:29 both of those contexts in terms of our
33:33 deal that we signed we indeed have
33:35 already ordered from CytoDyn our first
33:39 lot of pro 140 label with a fluorescent
33:43 dye so that we can sting tissues and
33:46 cells and say which cancer cells and the
33:49 immune cells associated with it and
33:51 which cells that HIV infects are
33:54 actually occupied by Pro 140 we actually
33:58 have the ideal tool to go to the FDA and
34:00 say listen this drug is working and an
34:03 irrespective of the viral load we know
34:06 this drug is working some of the things
34:08 that we're seeing on the ongoing HIV
34:11 trials are fascinating because Pro 140
34:15 acts on the cells that HIV infects and
34:18 protects them from being infected the
34:22 hallmark of HIV is the destruction of
34:24 the immune system as we all know and
34:26 AIDS right if you preserve the immune
34:30 system you're fine you have a competent
34:34 immune system that's what pro 140 does
34:36 it doesn't go in and inhibit the virus
34:40 like some of these other drugs do which
34:43 happen to be a lot more toxic than ccr5
34:46 but it blocks additional cells from
34:49 being infected which is really the
34:51 hallmark that's the goal of what
34:53 everybody should be looking for a good
34:55 analogy is I relate to you trying to
34:57 start a fire on your grill and you have
35:00 no charcoal but you have lighter fluid
35:02 so sometimes the lighter fluid will
35:05 light which I relate to an increase in
35:07 viral load but there's nothing to
35:10 propagate the fire so that you can cook
35:13 your hamburgers
35:13 right leronlimab
35:16 blocks the key cells that propagate
35:19 infection you need to prolonged
35:21 increases of viral load that's the
35:24 message that has to go to the FDA that
35:26 this drug is completely occupying the
35:29 receptors that it needs to occupy and
35:31 it's blocking virus from binding to
35:33 uninfected cells and preserving the
35:36 immune system that's where we all want
35:39 to be and in cancer ccr5 has been around
35:43 for a long time and it's not about ccr5
35:46 on the tumor
35:47 it's about ccr5 on certain immune cells
35:51 that that control the tumor okay so
35:54 there's two eight billion dollar-a-year
35:56 drugs called opdivo and keytruda
36:00 made by Merck and BMS that bring back
36:03 your own immune system to fight off the
36:05 tumor but you know what happens after
36:08 three to six months they stopped working
36:10 why do they stop working well this whole
36:13 new wave of cells comes in to shut that
36:17 immune response off that's part of the
36:19 elegance of our body in controlling you
36:23 know a immune response gone awry right
36:26 but in cancer we want the immune
36:28 response to go awry right those immune
36:32 cells called T reg cells that come in
36:34 and supposedly shut off the light switch
36:37 that opdivo and keytruda have turned back
36:40 on Express ccr5 so if we get pro 140 it
36:45 can block those cells from coming in and
36:48 shutting off the immune response that
36:50 you just spent two hundred thousand
36:52 dollars a year to bring back in the
36:54 patient it's a tremendous opportunity
36:56 this is a immuno oncology drug it is it
37:01 always has been and you know it hasn't
37:04 come to the forefront until just
37:06 recently now that we have more
37:08 information on how this immune response
37:11 against tumors is is regulated the other
37:14 thing that pro 140 does is it
37:16 reprogrammed
37:17 a cell called a macrophage think of
37:20 pac-man that little guy that goes around
37:22 and gobbles up little things on the
37:24 computer game
37:25 well macrophages come and gobble up
37:28 tumor cells normally right but when
37:31 they're when they're blocked by CCL 5
37:34 which is a protein made by t-cells they
37:38 don't go and gobble up the tumor cells
37:39 when you block with pro 140 those
37:43 macrophages are now active against the
37:45 tumor again so this is extremely
37:49 exciting immuno Oncology drug and you
37:53 know what I think the field is just
37:54 starting to realize it it's the
37:56 quarterback of cells moving in the body
37:59 to where they need to be and prolong for
38:02 taking control of that and now we have a
38:05 diagnostic that says this drug is going
38:07 to bind exactly in the past we've been
38:11 looking at ccr5 expression with antibody
38:13 bodies made by Dickinson and
38:15 other companies the problem is that
38:18 doesn't bind to the exact site that Pro
38:20 140 does so what we did in our deal is
38:23 we made sure that when we're doing
38:25 Diagnostics to see if there's a
38:27 candidate for pro 140 we're going to use
38:30 the actual drug as a diagnostic it's
38:34 elegant it's extremely elegant and it's
38:37 going to be much more specific and
38:39 accurate in defining the patients that
38:41 are going to respond and at the end of
38:43 the day we're all going to benefit from
38:45 that so I can't tell you how excited I
38:48 am about this and when you look at these
38:50 boards and all the different indications
38:51 it's easy to say well we're all over
38:53 the place in reality we're not what
38:56 we're just doing is taking advantage of
38:58 all the different disease states that
39:00 ccr5 is active in and this drug has
39:04 applications for all of those yet we
39:07 need to focus on the ones that are at
39:09 hand and get the HIV applications
39:12 approved but after that the pipeline
39:15 after that they'll just keep feeding
39:17 keep feeding the utility of pro 140 is
39:21 extremely excited really really exciting
39:25 both for the emulation standpoint and a
39:28 viral logic standpoint and again
39:30 for my work at Northwestern first and
39:33 then at Stanford this is what I spent my
39:35 life doing and finally this is coming to
39:38 the forefront so and I'm happy to answer
39:40 any questions any time show you any data
39:44 that we have internally that may not be
39:46 out to the masses or out to the FDA yet
39:48 because it is really really exciting
39:51 when I'm looking at this data coming off
39:53 our machines every single day there's
39:56 not a single day where I can't wait to
39:58 get into work and see that so we
40:09 definitely answer any question
5
