Greetings and Welcome Here.

So the last post brought up a prior discussion Dr. Lalezari had with some college students regarding CD10 mostly and some of CD12. Those were the (2) COVID-19 trials CytoDyn did. There is a stark difference between what Dr. Lalezari was convinced to believe and what the end results became. Dr. Lalezari was there first hand and he appreciated what took place first hand and so he formed his belief system around the actual results.

The interview took place in October of 2020, so, it is over 4 years old and since then, despite what has been said or written in the past 4 years, Dr. Lalezari has not changed his mind or regretted anything he has said in regards to how well leronlimab treats COVID-19, because he knows assuredly, that this disease is a RANTES disease.

I brought this up again, this 4 year old video, I re-hashed it primarily because of the recent paper that was released on the CD10 trial referenced here. It is only in partial form and some snippets are provided, but it suffices to contribute to the fact that COVID-19 is a RANTES disease. This information must be precedented to know the facts and not the lies which have been more widely disseminated. It is provided to reinforce the need to stick with the truth being released now in peer-reviewed published manuscript articles.

Lalezari was present on the front lines of executing CD10 himself. He was a Trooper fighting the war against the disease. With CD10, he saw the actual signal that leronlimab was in fact functioning and executing in COVID-19. These are his words:

"... so I am stunned to see that even in patients with Mild to Moderate illness, leronlimab seems to be having a very significant impact and clear signal of activity and that is the Primary Endpoint now."

Why did he have that signal?

"... So we found that patients who had a score of at least 4 on day one, meaning they weren't folks with no symptoms. We had no real effect on patients with no symptoms. Those people tend to get better on their own. But patients who had a score of 4 or more, we reduce symptoms at day 3, from 90% to 70% which is moving the needle*..."*

Remember, the patients in this trial were only Mild to Moderate. They did not have development of large amounts of CCR5, but despite this, leronlimab still had an impact in the prevention of more severe disease. I stated in the linked post:

"Leronlimab is disease agnostic, variant agnostic and leads to improved healing, better health and longevity and even protects against inflammatory diseases including cancer, arthritis, Alzheimer’s and many others.

Leronlimab is agnostic to pathology. It is not specific to any, rather applicable across the broader spectrum of inflammatory disease."

How was this recognized? The signal that Dr. Lalezari recognized was NEWS2.

"JL 31:11: Specifically, there's a thing called a NEWS2 score which is a National Early Warning System score developed by the Royal College of London in England and it's a score that predicts pulmonary collapse. So, who's going to end up being intubated in the ICU and it includes things like Respiratory Rate, oxygen saturation, blood pressure, level of consciousness and so on. Seven metrics and this NEWS2 is becoming a very critical End Point in a variety for multiple sponsors. Because, what we really I mean yes, we want to lower muscle aches, but what we really want to do is prevent people from ending up in the ICU intubated and dying*. So this* NEWS2 predicts who's going to get into trouble. So if you look at the NEWS2 score on leronlimab versus placebo, we had a statistically significant result at day 3 and at day 14*."*

So, Lalezari knew that leronlimab could treat COVID 19 from the NEWS2 signal. Unfortunately, within months of this interview, his zeal for this discovery was not well received.

"With the conclusion of both the CD10 and CD12 clinical trials, it has become clear that the data currently available do not support the clinical benefit of leronlimab for the treatment of COVID-19*. In the smaller study that CytoDyn conducted in patients with* mild-to-moderate COVID-19 disease (CD10), there was no observed effect of the drug on the study’s primary endpoint or on any of the secondary endpoints*. The primary endpoint for the CD10 trial relied on a measure of participants’ COVID-19 symptoms called a “total clinical symptom score”, which was assigned based on the severity of each participant’s fever, muscle aches, shortness of breath, and cough. This score ranged from 0 (no symptoms) to 12 (all 4 symptoms present and severe).* The CD10 trial results showed no clinically meaningful differences in average change in “total clinical symptom score” from baseline to Day 14 between study arms (-3.5 in the leronlimab group versus -3.4 in the placebo group). Additionally, none of the secondary endpoints were met in this study, including mortality, time to symptom resolution, and time to return to normal activity. Taken together, the CD10 results indicate that most study participants experienced resolution in COVID-19 symptoms regardless of whether they received leronlimab or placebo.**"

So with respect to CD10, this statement by the FDA is true, but it fails to bring up NEWS2 because the discovery of NEWS2 was post hoc as stated in the recently published paper. Dr. Lalezari acknowledged that CD10 did not meet Primary Endpoint. He told that in this interview to the college students. He also told them about NEWS2, which the FDA completely neglected during this dire time when millions of Americans and tens of millions world wide met their early death due to this disease.

"Findings

Overall, 84 participants were randomized and treated with leronlimab (n = 56) or placebo (n = 28). No difference was observed in change in total symptom score (P = 0.8184) or other pre-specified secondary endpoints between treatments. However, in a post hoc analysis, 50.0% of participants treated with leronlimab demonstrated improvements from baseline in National Early Warning Score 2 (NEWS2) at day 14, compared with 20·8% of participants in the placebo group (post hoc; p = 0.0223). Among participants in this trial with mild-to-moderate COVID-19 adverse events rates were numerically but not statistically significantly lower in leronlimab participants (33.9%) compared with placebo participants (50.0%)."

Post hoc means that it was determined / discovered after the trial completed. It was not considered as a Primary Endpoint from the get go, but, in hind sight, it should have been, but nobody understood COVID-19 at that point in 2020. After seeing the results, Dr. Lalezari could not dismiss these findings. The data were there in front of him.

"... We conclude from CD10 that there's no question but that there is a signal that leronlimab is working in Covid 19. It's no longer a question of is it working. It is. Now the question is how well is it working. We are unable to answer that question based on the results from a mild to moderate population because those folks just aren't sick enough for us to really put the drug to the test*.*

JL 35:10: The test will be CD12 where patients are in trouble ...

... yeah, so what we know is leronlimab works in Covid 19 and it is utterly amazing that we're doing this interview today because I can make that statement and I know it's true and I know it's true for two days now and the world doesn't realize it yet. We have to break through a lot of media fog but it is true and in as we see CD12, we'll get again know whether it's a single, double, triple or home run and then there are questions of well where are we going to use it."

We all know the story of CD12. His zeal was justified if you consider now the findings of the recently published paper on this topic.

Introduction of the newly released manuscript was made in The 5/30/2024 Webcast:

"In addition to that. now published data, we have two manuscripts from our studies of patients with triple negative breast cancer, a manuscript from our study of HIV positive patients with multi-drug resistant virus, and a manuscript from our study of patients with mild to moderate COVID-19 that have all been submitted from publication and are currently undergoing peer review. In addition, a manuscript detailing results from both our pre-clinical and clinical studies of leronlimab in MASH is undergoing final internal review and will be submitted shortly."

Excerpts coming from the Published Article "A Randomized Placebo-Controlled Trial of Leronlimab in Mild-To-Moderate COVID-19" follow:

The TEMPEST trial was a randomized, double-blind, placebo-controlled study in participants with mild-to-moderate COVID-19. Participants were randomly assigned in a 2:1 ratio to receive subcutaneous leronlimab (700 mg) or placebo on days 0 and 7. The primary efficacy endpoint was assessed by change in total symptom score based on fever, myalgia, dyspnea, and cough, at end of treatment (day 14)**.

However, in a post hoc analysis, 50.0% of participants treated with leronlimab demonstrated improvements from baseline in National Early Warning Score 2 (NEWS2) at day 14, compared with 20·8% of participants in the placebo group (post hoc; p = 0.0223).

However, the results of the exploratory post hoc analysis showing that participants in the leronlimab group had greater improvement in NEWS2 assessment compared to placebo provided a suggestion that leronlimab may be associated with a lower likelihood of people with mild-to-moderate COVID-19 progressing to more severe disease and needs to be confirmed in other appropriately designed clinical trials.

CD10 Clinical Trial Results

Moreover, people with the CCR5-Δ32 gene variant, which decreases cell surface expression of CCR5 and attenuates pro-inflammatory responses, were shown to have a significantly reduced risk of severe COVID-19*.*

Collectively, these findings provide compelling evidence that hyperactivation of CCR5 contributes to the pathological inflammatory response seen in severe and critical disease and highlight CCR5 as a potential therapeutic target in COVID-19.

Recently, several case studies of people with severe or critical COVID-19 demonstrated that leronlimab treatment was associated with a reduction in elevated plasma IL-6 and CCL5, normalized CD4/CD8 ratios, and was associated with high rates of recovery, suggesting clinical benefit*.*

These excerpts prove that what Dr. Lalezari was saying 4 years prior to the peer-reviewed publication was spot on. Now, the published manuscript says so. He knew it all along, as did all the long shareholders. The peer-reviewed published manuscript validates that leronlimab could have effectively provided clinical benefit even to patients with mild to moderate COVID-19, (mild to moderate levels of CCR5). Essentially saying that leronlimab could be used as a prophylactic medication in COVID-19, to ward off more severe disease. Will that be pursued? Will another corona virus come to destroy the world?

So where is CytoDyn going today? November 16, 2024?

"These last five months have been really utterly awful and I know I have PTSD from it and in part it's awful because we didn't go into this in detail, but we actually knew leronlimab was working back in March because there were various doctors and families around the country who had called and said they wanted you know emergency access to leronlimab through the right to try program and so the FDA issued individual investigational new drug approvals for about 85 patients who were then treated at various hospitals around the country in New York; in Georgia; in Los Angeles and we were able to collect data on those patients and we knew we CytoDyn knew that the drug was working back in March and certainly in April and we knew it was working before we knew how it was working and we certainly knew it was working before everybody started dying and there wasn't any way to break through the media, the government, the FDA because nobody believed us because there are a hundred companies out there saying we have the cure to Covid, but we knew we did not necessarily the cure, but we had an effective treatment, because even though these were not randomized patients, normally you have to do a randomized study in order to remove hidden biases, so that your treatment and placebo groups are balanced for things that you know about and things that you don't know about. Well, we didn't have a randomized arm control arm, but we were treating the patients who were on death's door so there wasn't a lot of, you know, randomization bias. If anything, we were treating the sickest of the sick and a lot of these folks died, but we looked at their lab results and before they died they were able to show us that the drug was working in that we saw reduced levels of the cytokine IL-6. We saw increases in the CD8 counts and balancing of the immune system and so there were a bunch of people who died and the last thing they did before they died was show us at CytoDyn that the drug was working, but nobody would believe that data because it wasn't really randomized data and nobody acts on data without a control arm.

JL 54:00: So we have had to hustle you know, to get the CD10 study, the CD12 study, first approved by the FDA and then we had to get them enrolled, which was incredibly difficult in an environment where Gilead and other large companies rose, Genentech, were doing their own clinical studies and and just had far more resources than this little company CytoDyn which started as a nickel, 30 cent stock. They just didn't have the money to throw at this the way a big company would and certainly NIH and our government, nobody has helped CytoDyn with anything. So, it was extremely traumatizing to to look at the results from the emergency IND patients, be pretty sure we had a treatment that was working, even in patients who were really ill, and then to not even know exactly how it was working, which cells it was affecting trafficking, or but then to have to start from scratch, while you know we're hearing reports like there are not enough ventilators in New York and then to see 150 probably closer to 200 000 people now die and just in the US, while we have been scrambling to get these studies filled, enrolled and then now analyzed, it has been psychologically and spiritually exhausting and there's really nobody in a position of any authority that has helped us at all and I'm trying not to be bitter about it.

56:00: Okay. Thank you. Do you have any closing remarks for us today?

JL 56:07: I just say thank you. I enjoyed talking with you. I'm sure I ran on more than you anticipated. Certainly more than I anticipated. It's incredible that you asked to do this interview this day. I know one thing. I've learned about Covid is I've had to learn to trust the process*. There's a hand in the universe. Mama gaia, she's got it.* Things are happening for a reason sometimes we don't understand why*. I actually want you to know. It means a lot that we did this interview today because these feelings that I'm having* this information that I'm sharing is both raw and fresh. You know we've submitted to the FDA now and we're submitting to the regulatory authorities in England, in Mexico, Brazil hopefully Israel and and you are about to hear more about leronlimab in the coming weeks and or month, six weeks, you know CD12, certainly by October first. Hopefully, but no one right now knows about it except you and me and a few other people and CytoDyn's investors. So, it's incredible that we've had this opportunity and I'm grateful to have had this opportunity to share this with all of you."

Can you relate to Lalezari? What were his instincts then? His instincts haven't changed. Maybe he is now more disciplined, but his instincts are the same. So then, Where is this published paper going? England, Mexico, Brazil, Israel. What should CytoDyn Investors be looking for? More of these sorts of peer reviewed published manuscripts, because they go round the world. These papers are the proof of what CytoDyn knows as truth. So let it be known world wide what CytoDyn knows first hand. It gives validity to CytoDyn's partners that the moves they initiate are well founded and may be banked on to create a medication in combination capable of re-creating the effects of the CCR5 delta 32 mutation. The peer reviewed papers declare leronlimab's inherent and proven effectiveness and safety. Partnership is fostered.

The papers shall continue to come. The partnership shall also come. Lalezari knew 4 years ago, leronlimab treats COVID-19. The paper today proves it. Let's stick with what the papers say so we can know what is coming next.