The Investment Idea Behind It All
The bet is that an investment in a biotech, CytoDyn (CYDY), with a single drug with multiple applications will find its markets, generate billions of revenue, save lives, improve the quality of life, and deliver an unusually high return to investors.
The interviews were done between July 8 and August 20.
Results of a
Mild-to-Moderate Covid-19 Study Were Excellent
CytoDyn has
just completed a statistically significant Covid-19 study of mild-to-moderate
subjects a week ago. The results were
unusual on the safety end. Basically,
you were at twice the risk of a SAE (severe adverse event) if you were in the placebo
group. 5 SAEs out of 56 for the
leronlimab group versus 12 out of 56 (2x of 6 out of 28) in the control
group. In the usual case, an
experimental drug hopes their safety will be as good as the control group
(placebo). This kind of thing where the
safety of the experimental drug is much better than control does not happen,
according to Jay Lalezari, CytoDyn Interim Chief Scientist. So, it appears to be very safe indeed.
The efficacy
was also outstanding in this study of patients in which both the control group
and the leronlimab group are recovering from Covid-19 infection. Against a standard called NEWS2, leronlimab
subjects saw 50% improvement versus 20% improvement by the placebo group.
Consequently,
CytoDyn has applied to the FDA for right to sell the product under an EUA, an
emergency use authorization for an unmet medical need. The government is under pressure to provide
medicines against this malignant virus, but the problem is that even though the
FDA authorized this small Phase 2 study of 75, they did not intend to approve
it for sale on the basis of such a small study.
So, they have to decide in this time of crisis where 10,000 people are
dying each month whether to give it the green light, or hold out for more
results. It will require nerves of steel
whichever way they decide. Usually, FDA
requires a larger Phase 3 to further establish the good results of a Phase 2
study. So, approval is not in the
bag. It is typically a matter of numbers. Working in their favor are the excellent
safety results so far. More than 800 HIV
patients have been tested with no death or serious complications. And now there are more cancer subjects added
to that, and the unusually good safety results of the Covid-19 patients.
When the CEO
Dr. Nader Pourhassan was queried about doing another trial for FDA, he’s not
bothered. A double blind study has just
been completed in which the results were wonderful, indeed all of their trial
results have been positive. Though
sensibly they have pursued trials where the receptor CCR5 was implicated and
studied and written about in the medical literature, so there were theoretical
reasons to believe it might work.
Small
biotechs are always short of cash, but CEO Pourhassan reports by virtue of the
exercise of warrants, and a recent funding of $28.5 million at a conversion
rate of $10 means that he has never had so much money in the bank.
Below are
interviews with the CEO of CytoDyn, Nader Pourhassan, and the Chairman of the
Board of CytoDyn, Scott Kelly. As the
interviews will show, Pourhassan has the essential qualities of an outstanding
CEO, a Ph.D. himself, he tracked down the best brains he could find, and
learned from them. When advisors were
hesitant, he went ahead anyway, and was proved correct. And when an inquiring doctor called the
office asking about this possibility and that possibility, he recruited that
doctor (Scott Kelly M.D.), who eventually quit his practice and joined the
Board, eventually becoming Chairman, but staying true to his own north star, the
drug’s possibilities, he took the additional job of Chief Medical Officer.
It is
important to explain the word “indication”.
An indication in biotech means
the possibility that a given medical condition may respond to a medication, in
this case we are speaking of CytoDyn’s leronlimab.
The
Interviews
Thomas Barnard: So let's see, where shall I begin? How is your mother-in-law? [CytoDyn investors will know that she was the first lady with mTNBC – metastatic triple negative breast cancer – to receive leronlimab.]
Nader
Pourhassan: Doing much better than she was doing a few weeks ago.
Thomas
Barnard: What happened?
Nader
Pourhassan: She still has tumor
in her brain, and she had a mild stroke a couple of weeks ago. It affected her right side, and the doctor
said she would never be able to use the right side, and it won’t come
back. But within three days she was able
to walk on her own. Slowly, of
course. Scott Kelly found published
papers on CCR5 and stroke.
Thomas
Barnard: What about her
right arm? Can she do anything with
that?
Nader
Pourhassan: Yes, she eats with
her right hand, and she’s using it.
Thomas
Barnard: Wow.
Nader
Pourhassan: Yes, it’s
remarkable. We think it is the weekly
doses of leronlimab that is helping her.
It’s anecdotal, but we are having the doctor prepare a case report.
Thomas
Barnard: Home testing of a
new indication? So, let me ask you this:
How did CytoDyn connect with Bruce Patterson? I mean, did he see your work and
come to you or did you go to him or how did that work?
Nader Pourhassan: So Bruce Patterson was introduced to us through an
associate of one of our old board members. And then I talked to him right after
I heard about him. When I met with him he said he could do receptor occupancy
tests for us. He could develop an assay for us and while we had other people
who could do receptor occupancy tests, we went ahead and gave the project to
him.
Thomas Barnard: A receptor occupancy test?
Nader Pourhassan: A receptor occupancy test tells you if the
leronlimab is sitting on the receptor.
Nader Pourhassan: And
he also was adamant that the cancer possibilities were great, but we were already
doing cancer with Dr. Richard Pestell, and before that with Dr. Denis
Burger. However, at that time, Dr.
Pestell was our Chief Medical Officer. Dr. Pestell had already helped us to get
the triple negative breast cancer trials under way. And when Bruce Patterson
joined us as a consultant, he said that there's a lot of potential here and we
were happy with that. In a few months we terminated Dr. Richard Pestell, and
only worked with Dr. Patterson. Dr.
Pestell gave us some fantastic information on receptor occupancy of cancer
patients. It turns out that Dr.
Patterson was not able to get the assay ready for receptor occupancy. So we got another lab, which was
run Hallgeir Rui, M.D. Ph.D. So any cancer patient today who wants to get
involved in the leronlimab trial must first have a biopsy. And then we send the biopsy to Dr. Hallgeir
Rui, whose laboratory is in Wisconsin. And over there they analyzed to see if
we have the necessary receptors. I mean, if the patient is qualified to
be in the cancer study.
Thomas Barnard: So, let me
understand, what you mean is that cancer must show the CCR5 receptor or
forget it. Right?
Nader Pourhassan: The cancer
patient’s biopsy is checked for a few things.
First, does it have CCR5 on any of the tumor cells? And then there's
infiltration of the leukocytes around the tumor cells. Do the leukocytes have
any CCR5? And we checked both of those. Now, if they do, they're qualified to
be in the trial.
It was around this time that Dr. Scott
Kelly started asking me about what do you think about Covid-19 because he
thought that ARDS was something we might work on, and which we had already
discussed with other folks. I called Dr. Patterson. He also agreed that yes,
you will be able to stop ARDS, which is the main cause of death in
Covid-19. We immediately prepared IND
and protocol and sent it to the FDA for a phase 2 trial. They said, no, you can’t file IND, you have
to do pre-IND first, because you don't have any data. And that's when we got a
call from Dr. Seethamraju. He said, My
critical patients are not doing well at all. They are not going to make
it. He called FDA and said, I agree with
that theory leronlimab stops the trafficking of macrophages that was published
in articles. So once he injected patients under an Emergency IND that
made FDA feel more comfortable that our drug was not going to increase the
cytokine storm, but perhaps give some benefit.
After a couple of patients were extubated, they immediately gave us
Phase 2 and Phase 3 green light without waiting three months or so.
Thomas Barnard: That's very interesting to know. So it was actually
Scott Kelly, your Chairman and Chief Medical Officer, who was the one who
thought working on Covid might be a good idea.
Nader Pourhassan: Yes, that's correct. But not only him, but there were
other people who were telling me about it. We were talking to a company - I
don't want to use their name, but a company, their chief medical officer, a
very close friend of mine said we're looking at flu and you guys should probably
have indication in flu. And I spoke to
Dr. Denis Berger, who was a board member. And he's the one that conducted the
study for M.S. [multiple sclerosis]. He
had friends at the Providence Medical Center. After seeing the results of the
animal study he thought M.S. is a huge indication. But
it was Dr. Denis Burger, a former professor at Oregon Health and Sciences
University, who had pointed to [M.S.] for many years, and he was the
CEO for four successful biotechs. And I'm still in touch with Dr. Denis Burger.
So the increase in the number of indications that leronlimab were found to have
was because of Dr. Denis Burger and Dr. Scott Kelly. I had asked Dr. Burger about the cancer
indication many years ago. And that's when we filed for patents for cancer (he
is the inventor on many of our cancer patents).
That was four years ago, it three years later, we got to know Dr.
Patterson. Then we got started with Dr. Jay Lalezari in cancer. Dr Jay Lalezari was always involved with us
from day one, but not in cancer originally, in HIV.
Thomas Barnard: Gotcha. Let's go back to the breast cancer thing, that
was actually the thing that that moved me to buy shares a while back, because I
thought that was an extraordinary result. Now I'm reading up. And it seems like
Pfizer has a drug called Maraviroc, which they wrote about it in February of
2019. So that would seem to have indicated that when you tried it out on
your mother-in-law, it wasn't out of the blue, you had a foundation actually
that this might work. Is that right?
Nader Pourhassan: So, yeah. So Pfizer had started a cancer trial with
Maraviroc, I believe, several years ago. And they started even before we
did. As I told you at the beginning,
about three or four years ago we applied for patents with Dr. Denis Burger. So
Pfizer accidentally found all these new indications in graft versus host
disease for Maraviroc. How was that? Well, the patients who have HIV for a long
time usually develop AML, acute myeloid leukemia, or DMS, and they need bone
marrow transplant. When Pfizer looked at the data they realized that these
patients who get bone marrow transplant don't get graft versus host disease if
they were HIV patients who were on Maraviroc. They all of a sudden say,
wait a minute, this might have indication. Maraviroc might have indication in
GvHD [graft versus host disease].
Thomas Barnard: (laughing) I see. By accident.
Nader Pourhassan: Let me tell you the most interesting part at that
time. At CytoDyn we had a very strong cancer person, key opinion leader. And
that person and Dr. Denis Burger both believed in the potential GvHD indication
for leronlimab (called PRO 140 at that time).
I wanted to do an animal study of graft versus host disease with
leronlimab. When we held a key opinion meeting Dr. Paul Maddon, inventor, was
on the call at my request. I had asked him to come on the call. He said no, no,
no, no. There is no GvHD [graft versus host indication] for leronlimab. This was four and a half, five years ago. And
he said, No, no, no, everything must stop. Maraviroc stops chemokines from
binding. Leronlimab doesn't do that. And that's why we don't have any side
effects or toxicity. So stop everything. Everything gets stopped, and the next
day or two I told Denis Burger: I
want to know why the video that shows mechanism of action of leronlimab by Paul
Maddon had indicated that chemokine binding hardly doesn't happen. “Hardly”
doesn't mean zero in mathematics. Hardly means something. Need to go check with the company who did the
toxicology of leronlimab and find out what amount of PRO 140 [leronlimab] do we
need to use to make that happen? And Dennis Burger said, no, no, no,
leave it alone, you don't know what the hell you are talking about. Stop it.
Dr. Bruce Montgomery (a board member at
that time) says no. Paul said no. I
said, Well, I'm going to get it myself. So I had Amarex call Nobel
Lifesciences, Dr. Stephen Horrigan. He knows me very well from that time,
because I thought, I'm doing this without my board members support. And I sent
twelve thousand dollars to do the in vitro study. And this study showed that
leronlimab was better than Maraviroc in GvHD in an in vitro study. I had Amarex send the data to the FDA without
the board members approval and submitted a protocol. And Denis Burger said, Oh
my God, you were right. And FDA immediately gave us Phase 2 and asked for
animal data in order to give us Orpha Drug Designation. So I told Denis Burger,
Please now go do the animal study that the FDA is requesting. The FDA suggested that in our animal study
that we inject 32 mice with human bone marrow. We knew they all would die from
GvHD. If some of the mice in the half
(16) that get leronlimab stay alive, we’ll give leronlimab Orphan Drug
Designation. All the mice stayed alive! And all the mice in the control arm
that did not get leronlimab died. And Denis Burger said, “Oh, my God,
leronlimab has potential for many so many things.” Dennis Burger became my hero at that time
because he was forced to stay with GvHD by me, and that opened the door for him
to explore M.S., cancer, and many more indications for leronlimab. I loved Denis and still do.
And then he took the product to
Providence for an animal study in M.S., and he cried almost at the board
meeting. The three mice that got
leronlimab had zero paralysis.
Zero. And the people at
Providence Medical Center said, Where did you get this product? Oh, my God. And
then Dr Jonah Sacha said, “Nader, every time we show the results of leronlimab
to the scientists, they say where did you get this product? This product is worth billions and billions.
This is unbelievable what it can do for humanity.”
Thomas Barnard: Good. So I'm understanding then that leronlimab works
better than Maraviroc.
Nader Pourhassan: Absolutely. Maraviroc has approval for HIV. But it has
a black box warning, it has liver toxicity. Our product, we believe, probably
helps with liver restoration; it helps all kinds of different autoimmune and
cancers. So, if our bodies suffer for
whatever reason, any virus, Covid-19, flu or whatever, or any scratch or any
foreign object goes your body…the immune system must fight it. Many of our immune cells have CCR5 on their
surfaces - macrophages and on T regulatory cells. And we believe that probably
leronlimab binds to a very, very special place on CCR5, which is a work of art
by Dr. Paul Maddon and William Olson, Ph.D. from MIT.
Thomas Barnard: Did Maddon know what he was doing when he did this? I
mean, did he…
Nader Pourhassan: He was focused on getting this molecule to bind to the
exact location that HIV binds. Just keep in mind, Paul Maddon got his M.D. and
Ph.D. from Columbia University, his dissertation, his research for his Ph.D.
was on where HIV binds first, which was the CD4 receptor on a T-cell. So he was
the first man who discovered that. Then,
he founded Progenics, a biotech company. And then he discovered the interaction
of HIV with CCR5. Then he made an antibody against CCR5. And Dr. David Ho, who
ended up saving millions of lives of HIV patients by developing HAART and became
Time magazine Man of the Year, was a very close colleague of Dr. Paul Maddon.
Ho found an antibody against CCR4. Paul
Maddon felt he had a better target, and said, I want to go after CCR5. Now at Progenics, where he founded Progenics
and where he was CEO for 30 years. He
got the molecule to bind to the optimal site on CCR5.
He first found a molecule and it was
called (I believe) PRO 540, not 140. In
the first year of development of PRO 540, the viral load drop wasn't good
enough because it wasn't binding to exactly the right place. Dr. William Olson,
(Ph.D. from M.I.T.) worked for Dr. Maddon, said to me that not long after the
PRO 540 failure, We went back to the drawing board. I went through thousands
and thousands of antibodies, and one morning I came in and I had isolated one
antibody and I thought, my God, it binds to one hundred eight point percent of
the HIV binding sites. That would mean
that HIV would have no way to bind to that site.
He said immediately when they got that
molecule they had to humanize it, which cost them a lot of money in 1999. And
we, CytoDyn, still pay a royalty because of that. And they immediately went to
the clinical trial and boom! - it was safe even with people who did not have
HIV. Two trials were done on HIV negative
people. Very very safe. The FDA gave a fast track designation based
upon the safety and then Progenics did a Phase 2a and the viral load drop was
one point six logarithm in just one week. Dr. Jeffrey Jacobsen from Jefferson
University said that the viral load drop we saw for PRO 140 was better or as
good as any HIV drug they have ever seen
(at that time).
So, Dr. Paul Maddon stepped down as its
CEO due to a lot of things including his own personal life. And immediately the
new CEO said, what's the path to approval for PRO 140?
And the company said to him, well, you
know, we need to do a Phase 2b. Well, how long does that take? Fifteen years.
Ten years. The Phase 2b designed was in a substance abuse population. Then
after that you need to do a Phase 3 (similar to a Phase 2 but five to ten times
larger). In 2009 the FDA had told
Progenics - You have to do a phase three on top of that Phase 2b. So now you've
got 20 years of different trials to go through, and all of that for what
possible outcome?
Thomas Barnard: Ha, ha, right …
for substance abuse.
Nader Pourhassan: Yes, exactly.
That's a population worth maybe 20 million dollars revenue per year. And
then the new CEO took over… He said, sell this damn thing. And he was vulgar
about it. And when we went there to pick
up the product, he was saying, get this S-H-I-T out of here. Take every damn thing that has to do with
this. They had spent hundreds of millions of dollars on manufacturing. There
were eighty kilograms, equal to like half a million doses of this product,
which they had made, and which they had stored at negative 80 degree Celsius.
They sold all of that and they had NIH
money, $6 million, to conduct their Phase 2b substance abuse population. Dr.
Jeffrey Jacobson was in charge of that. He had published several papers on PRO
140 and done all the Phase 1, 1a, and 2a. So I met up with him and had dinner
with him several times. And I said, I'm not going to do this study. And he
said, what do you mean? You don't know
what the heck you are talking about. Who are you anyway? I explained that I had
talked to Dr. Robert Schooley who you know, and he doesn’t think that is the
way to go. Jacobsen says, Chip thinks that?
So he called Dr. Robert Schooley and he said, Yes, there should be a study
that compares leronlimab to Maraviroc or something like that. I had Chip
outline every possible path to approval (and there were 5 or 6 of them). And I
have a letter from him that I still keep for history [laughing].
He wrote to me and explained that I
asked him to write a letter outlining all the paths to approval for PRO 140 so
that I can share with the board. After
that we had an analysis done by smart analysts on all these paths and potential
revenue of each path should PRO 140 be successful in any of them. Smart analysts provided me with a ninety
thousand dollar report said that this product (PRO 140) has no value. The head
of Harvard University Medical School at that time said that this product will
never make any money. So I went to the board that day and all the board members
said, well, we're done. We should just shut down CytoDyn. And when they say there's no path forward, I
said, wait a minute, guys. I think I can change the HIV paradigm with this.
They ask me: What are you talking about?
Well, it's not me. Here's this letter from Dr. Robert Schooley. I put his
letter up on the screen. It was five or
six paths forward. And I told the board, I am choosing [HIV] monotherapy as the
path for leronlimab’s future.
Thomas Barnard: And this is...
Nader Pourhassan: So
I talked to one of the inventors [of leronlimab], Dr. William Olson, and he
said it was binding one hundred eight point five percent of the binding sites
of HIV. So why would anybody say it won’t work in monotherapy? I think it will
work. Dr. Robert Schooley says maybe it'll work and maybe it won’t. He said,You
don't know till you try it. So I'm going to try it. The FDA was not happy with
the idea of monotherapy. We also had to terminate our scientists who couldn't
help us with the regulatory path. It was me a mechanical engineer trying to
build something in monotherapy, and I only thought I had a 50% chance at
best. Though Dr. Robert Schooley
thought I had a chance, and also Dr. Jay Lalezari, who said, If this works
Nader, you’ve hit a homerun. And I said,
Let’s see. And we abandoned the NIH’s
grant of $6 million and went the monotherapy route.
Thomas Barnard: Robert Schooley, was he the guy that you called in
Africa?
Nader Pourhassan: [laughing] Yes, he was. I have tremendous amount
of respect for him. When you talk about top person in the world, for me, that's
Dr. Robert Schooley, Dr. Scott Hammer, Dr. Paul Maddon and Dr. Jay
Lalezari. These four people carried me
through this, especially Dr. Paul Maddon, who became my mentor and my very
close friend. We used to talk almost every day.
Thomas Barnard: Really? So you're
still in touch with the inventor then?
Nader Pourhassan: Absolutely. Yes, I love Paul. Jay Lalezari was very big also and still is,
and Dr. Scott Hammer was very kind to go to all the FDA meetings with us.
Thomas Barnard: How did you connect with Dr. Lalezari?
Nader Pourhassan: Lalezari’s dad,
Dr. Parviz Lalezari, read my book, which is called The Corruption of Muslim Minds. And he was also from Iran. A Jewish
Iranian guy who after the revolution also had a hard time like my Dad did. When he read my book and he realized I'm COO
of CytoDyn (at that time), he said - you should work with my son. So when I
checked his son out, I found he was a key opinion leader in a clinical trial.
So after I became the CEO, I asked Dr. Lalezari to help me and he agreed to do
so.
Thomas Barnard: So that's how you connected with him. So, as I understand it the breast cancer
trial is entirely composed of EIND patients or compassionate use patients?
Nader Pourhassan: No,
no. We have a Phase 1b/2 in mTNBC [metatastic triple negative breast
cancer]. In the compassionate use we
have over 10 patients enrolled. In the
emergency IND I have one patient, which is my mother-in-law. And then in the basket trial we now have six
or seven patients. The basket trail is
designed to include solid tumor data of 22 different cancers.
Thomas Barnard: Right. Right.
Nader Pourhassan: The patients that we have right now I don't
know exactly which cancers. But prostate cancer is one of them.
Thomas Barnard: That's good. Good. I mean, I'm a man. So now I'm happy
to hear that you working on that. You have a lot on your plate.
Nader Pourhassan:
We have one drug with maybe 30 different indications.
Thomas Barnard: In your capacity, let's say, as chief safety officer, we
are led to understand that over 800 patients have been enrolled in HIV testing
without death or serious complication. You told Dr. Mobeen Syed that there are
basically no complications with other drugs. That's what you said yesterday.
Many people are wondering to
themselves, since there have been over one hundred thousand deaths in the U.S.
alone, since you made your first announcement about a corona virus trial on
March 9th. And understanding that I am
asking this question within a very narrow frame, knowing that you must work
with FDA, that indeed you are a fan of FDA, but understanding the severity of
the disease, and understanding that I'm not asking you a policy question, but a
very narrow question about safety. Would
there be any harm in some kind of temporary approval to sell this drug until
testing is completed?
Nader Pourhassan: So that's a very good question. And let me say this,
if you're going to sell a product to, let's just say, five million people, what
kind of sample size would give you complete assurance that nobody is going to
get harmed from this drug? For five million, how many patients should I
use? Now, when you say you have 800. FDA
says 800 is great. And they've been very accommodating, allowing us to use the
data from previous trials, even though the data was intended for a different
indication. So they went out of their way.
Something that usually ninety nine point nine percent of the time they
don't do. They said for your combination therapy for [HIV], we would use your
monotherapy data safety because you don't have enough data. If you do want to get the data from
combination therapy it will take you five years. It took us three to four years for 50
patients in that population to be enrolled.
So with that said, now it comes to
coronavirus. Should they take some chances? FDA wanted us to go through the
normal path that they gave to 200 other applicants for Covid-19 treatment. They
said go through pre-IND, and then IND, which would take three months minimum.
They changed that immediately when they saw two patients from Dr. Seethamraju,
one of them extubated. And Dr.
Seethamraju immediately asked for nine more EIND’s. So FDA said good, it looks like you
have something. Go ahead and do your Phase 2 and do your Phase 3 if you can
help critical patient. They did that for hydroxychloroquine. They did that for
remdesivir where they gave around a thousand three hundred patients to be
studied even though their safety wasn’t really proven yet. With us, they accepted 390 patients for that
same scenario because for safety, they were a little bit more comfortable with
us, I'm guessing. I'm not putting words in FDA’s mouth. Then with regard to
Phase 2 FDA allowed CytoDyn to conduct a trial of 75 patients. Unfortunately, some of investors criticize
FDA unjustly. They complain, Why doesn't
FDA give us more? But FDA is expert at
that, they don't have just one person working. They have many, many experts
working there. And they have been doing this for many, many years. For us to go
there and say to them - What? Why not this, why not that? They are the people who run that show, and I
believe they do a good job. And the last thing I want to do is to second guess
the FDA, especially when I don't have all the data that they would have. We
have to give room to our agency [FDA] who is respected all over the world, and
whose findings are accepted everywhere in the world. We should accept their
decisions. Why? Because they have tremendous credibility. Let's be happy about
what we have in this country. Let’s enjoy that.
Thomas Barnard: So all right. So what you're saying is you really don't
want to respond on safety because you don’t have all the data FDA has, and
maybe you don’t have the expertise, and that’s their job. Okay.
Thomas Barnard Nader Pourhassan: Covid-19. You know that all these
scientists are still saying we don't know a lot of things about it. They are
saying that all the time. So they don't
know. How do they know? How would they know what leronlimab would do, even
though it has shown safety in HIV population? We need to have some kind of
safety on coronavirus. Just look at it very carefully. I don't know about those
things. I don't know what standard they had, but they’ve got 200 companies, and
don’t give approval to anybody unless they can pass the test. Do they want to
have more people dying [from a new drug] than what are dying [from Covid]. So
we have to go through the same rigorous steps and make sure that we comply. I
do that as fast as we can, and agree with the way the system is working.
Thomas Barnard: Okay. Thank you.
Nader Pourhassan
You know, I mean, we're almost there.
Thomas Barnard: I as I said in my question, you know, one hundred
thousand people have maybe died since you started your studies. What
harm would there be? I mean, I don't know the answer. I'm just voicing what I think a lot of people
are curious about. And what you're saying is safety requires numbers.
Nader Pourhassan: Safety requires numbers. And FDA is expert at that. If
they believe it is safe, then we can take that to the bank. When I say
that it’s safe, it’s just me, and I’m CEO and I believe in this company and its
drugs. So that is not something the FDA should take seriously unless I can
provide data and I have not done that yet but we are very close (in my opinion)
of doing so. They should take the data seriously, and data in Covid-19.
Thomas Barnard: I have read that
leronlimab has an indication for Alzheimer’s, what can you tell me about that?
Nader Pourhassan: I am going to
direct you to Dr. Kelly, who is both our Chief Medical Officer and our
Chairman.
= = = =
So, I connected with Dr. Scott Kelly and asked him about the
Alzheimer’s trial.
Thomas Barnard: We understand that an Alzheimer’s
trial is in planning or in progress. Can leronlimab get through the blood
brain barrier?
Scott Kelly: Nader and I were discussing effector cells
crossing the blood brain barrier in Multiple Sclerosis, and the possibility of
leronlimab working on Alzheimer’s. We believe
there is a neuroinflammation component to Alzheimer’s, and leronlimab can
mitigate the recruitment and immigration of immune cells across the blood brain
barrier. In addition, since
neuroinflammation, and CCL5, can disrupt the blood brain barrier, it would
potentially allow leronlimab to enter the central nervous system directly.
Thomas Barnard: How far
along is this work?
Scott Kelly: We
are pretty far along on the protocol.
When that is complete, we’ll apply for a Phase 2 study.
Thomas
Barnard: And the liver disease NASH, how
did that come about?
Scott
Kelly: Dr. Dan Lindner did a study at
the Cleveland Clinic, which showed a 3 fold reduction in hepatic steatosis in
the leronlimab group as compared to placebo.
Hepatocytes secrete RANTES, and CCR5 is present on both
stellate cells and hepatocytes. We also know that stellate cells are what
produce the scar tissue in the liver.
Thomas
Barnard: Stroke was mentioned somewhere as a possible indication.
Scott
Kelly: Stroke is a more recent
possibility. Doctors have been
discussing this with us, and we think leronlimab could work based upon the
relationship of CCR5 in stroke recovery as well as traumatic brain injury.
Thomas Barnard: The
results of the mild-to-moderate study were pretty straightforward. Very
good improvement (50% vs 20%) against the NEWS2 standard, but the surprising
thing, I thought, were the safety results. On the conference call Jay
Lalezari was saying that these safety results were exceptional. The
impression he left was that most experimental drugs were happy just to match
the safety results of the control group, much less improve on them.
Further, he was saying that this should be one of the endpoints of the study,
even if it wasn't planned that way at the study outset. I heard this and
rolled it around in my mind, and it seems to me one reason this might be the
case comes with the theme of these interviews, which is that leronlimab seems
to work against many diseases, and that the reason it was so safe was that
aside from dealing with the Covid-19 infection, it was perhaps treating other
conditions the patient may have had. Do you think this might be true?
Scott
Kelly: I think the safety results are
better in leronlimab than placebo in the Covid-19 population because the effect
of the virus is not limited to the lungs but affects multiple organs. It is a
multisystem disorder and that is represented in SAE’s and AE’s.
Thomas
Barnard: Those are caused by Covid-19,
but I’m wondering if other secondary conditions that patients have had before
the disease, and which contribute to a bad picture. Could those also be improved by leronlimab?
Scott
Kelly: That is also possible.
Thomas
Barnard: When the basket cancer trial was announced, I did not quite get the
connection to the CCR5 receptor, but I presumed there must be one, so I looked
them up one by one against the cancers mentioned in the press release, and I
found a study or studies related to every single one. There appears to be
just an awful lot of research on the CCR5 receptor. Have you found this
to be true yourself?
Scott
Kelly: Yes, absolutely. This is
research being conducted by scientists all over the world independent of CytoDyn.
Q: How
did you get involved in CytoDyn? Nader Pourhassan was tired of traveling
to China, or maybe his wife was tired of him traveling to China, and one of his
friends asked him to get involved in this company he was over-invested
in. When you did buy your first
shares?
Scott
Kelly: I believe it was 2016 when I
bought my first shares. But I was
following it as early as 2011. My
interest in CytoDyn rose because they were doing HIV. And I wanted to find the next company Gilead
would acquire. Gilead is a leader in HIV and their HIV treatments still make up
the majority of their revenue. I liked the concept of blocking the CCR5
receptor, because I believe it makes more sense to block healthy cells from HIV
entry. Why wait until the virus enters the cell and begins to make
billions of copies of itself before you decide to fight it? It doesn’t
make sense. I watched the CytoDyn closely for years to try and find a
reason the technology would fail either from an efficacy standpoint or safety
standpoint. It never did. The efficacy and safety continued to
astonish me. Once I realized the same receptor was involved in multiple disease
processes, I felt it was important to pursue those opportunities so I became
more involved to assist in those efforts.
At first
I spoke with Michael Mulholland, and I would ask him: What am I missing? Still wondering about safety and
efficacy. And then I would ask him why
they weren’t pursuing other possibilities for leronlimab, and he said I should
talk with Nader. And I asked Nader: What
am I missing? And he said, Nothing. And I asked him about all these other
possibilities, graft versus host, and others, and he said, Who are you? I am a doctor and an investor in
biotech. And he said, You will need to
sign an NDA [non-disclosure agreement], so I can talk to you. And, when that was done he explained that
others on the board were only interested in the HIV indication.
Nader was
interested in these other indications, and he told me the story of Humira,
which stands for “human monoclonal antibody for rheumatoid arthritis,” a TNF
blocker [tumor necrosis factor] which became one of the most successful drugs
in history. The story was similar to
leronlimab. He asked if I would join the
board. And I said that I had a medical
practice, and I would have to get back to him.
Eventually, I agreed to join the board.
There were all these indications and I felt many patients would benefit. And I needed to become more involved to
pursue those other possibilities.
Thomas
Barnard: So, when you were first bought
was it mainly for HIV? But you also knew
about some of these other possible indications.
Scott
Kelly: Yes, but I realized as I learned
more about the drug that were more indications for leronlimab than I had
originally seen.
Thomas
Barnard: And you bought more shares?
Scott
Kelly: Yes
Thomas
Barnard: I think it is a common
occurrence. I bought with the breast
cancer results and then I wrote a piece about four biotechs. CytoDyn was one of them, and I bought some
more after I interviewed Nader. But I
also wrote about Sorrento…
Scott Kelly: I have followed Sorrento, and have invested
in their company. The stock is up on the
news of the saliva test. I have been a
biotech investor for years. And as I
said, I was looking for Gilead’s next acquisition. I thought Gilead would acquire Kite, and I
also purchased Juno which was acquired by Celgene.
Thomas
Barnard: Wow! That’s impressive. Though I always felt CAR T was just too
expensive. $300,000 per treatment. And would be supplanted by something less
expensive.
Scott
Kelly: It is expensive, that’s
true. But I think there will continue to
be a use for it. The beauty of
leronlimab is that it can be used with any of these cancer treatments - chemotherapy,
CAR T, radiation, checkpoint inhibitors.
There do not appear to be any drug interactions.
Thomas
Barnard: I know leronlimab has these
three possible actions in cancer: 1) it
stops metastasis, 2) the anti-angiogenesis effect, and 3) the re-polarization
of macrophages, but the one effect that I thought would be in every oncologists
toolkit was that it stops metastasis. If
you stop metastasis, there are a number of ways to knock out the primary tumor.
Scott
Kelly: You’re right. In animal studies, it was 98% effective in
stopping metastasis.
Thomas
Barnard: Is there anything else you’re
excited about?
Scott
Kelly: We
are working on PrEP (prevention of HIV) through a once a month injection, and
cure in HIV patients who are receiving allogeneic bone marrow
transplantation. The only two patients ever cured of HIV received bone
marrow transplants with cells deficient in the CCR5 receptor.
Thomas Barnard: I
think I understand…if there is no CCR5 receptor, then HIV has no place to land.
Scott Kelly: That’s
right. One of people on our scientific
advisory is Gero Hütter, who cured the first HIV patient, known as the Berlin
patient.
Thomas Barnard: That’s
handy.
Scott Kelly: Another
is Hope Rugo, who is a famous breast cancer researcher at UCSF.
Thomas Barnard: Also
handy, since you doing a trial on triple negative breast cancer patients.
Scott Kelly: The
prognosis for those patients is not very good.
Thomas Barnard: So
far it looks like leronlimab can help. Thank
you, Dr. Kelly.
The Indications
The
indications for leronlimab so far include HIV (where studies are completed and
an application for sale has been made to the FDA), Covid-19, multiple sclerosis,
graft-versus-host disease, breast cancer, and other cancers expressing the CCR5
receptor, influenza, stroke, and Alzheimer’s Disease. A small 30 subject Phase 2 trial is on-going
to test the drug against 22 different types of cancer.
Precision
Medicine
We
are in a new era of “precision medicine” based on an understood method of action. CytoDyn’s results appear to affirm that kind
of understanding:
Covid-19
– viral load drops to zero/undetectable
HIV
– viral load drops to zero/undetectable
Triple
Negative Breast Cancer – CTC’s (circulating tumor cells) drop to
zero/undetectable
Animal
studies also seem to confirm these kinds of results. In Multiple Sclerosis all of the control
animals that did not get leronlimab, were paralyzed. All the animals that got it were okay. In GvHD (graft versus host disease) all the
animals that got the leronlimab lived, all those that did not died. These are striking results.
Former
Director of Virology at Stanford, Dr. Bruce Patterson, said in his TEDx Talk,
that this is the kind of drug that the nation should be stockpiling against the
next viral outbreak. Time will tell.
