I want to to highlight a couple of things, for the

I want to to highlight a couple of things, for the lazy and impatient (which classifies most of the non-short, non-BP mole detractors on here):

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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 [NP] 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.

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You malcontents don't DESERVE the success that's coming your way.