Unmasking the Mechanism
Tumor cells are "non-self". They deserve to be destroyed. Should they not be destroyed, then they would overtake the body and ultimately destroy it. Therefore, the body must destroy the tumor if the body is to survive. Because of the Tumor's ability to speak to the Militia of the body, the Lymphocytes, White Blood Cells, Natural Killer Cells, CD8 Killer T-Cells, CD4 T-Cells, B-Cells etc.... it can cunningly convince this Militia that the Tumor is actually part of the body, that it is "self" and that it is not "invader". Should it succeed in this bio-chemical and inter-cellular communication challenge, then the Tumor would eventually succeed also in overtaking the body to the ultimate end of killing its host. To avoid this fate, we have devised bio-chemical mechanisms, monoclonal antibodies, which do interfere and reverse this inter-cellular and bio-chemical communication that the Tumor utilizes to its advantage to Escape the body's Immune defenses.
Two time tested individual and distinctly developed mechanisms may together work in unison thereby merging yet into a distinct third mechanism that overcomes the Tumor's lies and overcomes the Tumor. Going back to my old post, "Tower of Babel Thesis", the issue at hand, is that I failed to realize at the time that the Tumor could learn another language. I thought only one inter-cellular language was used, RANTES. But in fact, in a more recent Tumor Tower of Babel, two languages are used by the Tumor. In the first Tower of Babel, I discussed only one RANTES language but now, it has become evident that Tumors speak yet another language, completely exclusive and separate from RANTES. Tumors have the ability to suppress the Immune System by communicating on the PD1 axis by speaking PD-L1 to the ears of the Killer Cells.
So, in my original thesis, leronlimab is used to control and calm the Tumor, to straighten the waywardness of the Tumor. When leronlimab comes on board, it takes control of the situation and reduces the Tumor down even to imperceptible levels, not directly, but by recruitment of the appropriate natural and innate Militia of the body. With these system actually doing what they were meant to do, in a short time, as the body does work quite quickly, MRI scans could show no evidence of the Tumor, no evidence of disease NED. Subsequently, patients no longer complain of any Tumor related symptoms.
So leronlimab is a monoclonal antibody CCR5 Inhibitor and when CCR5 is blocked, the Tumor shrinks back. The Tumor shrivels and shrieks. The body no longer remains a good habitable dwelling place for it. But leronlimab does this work not by attacking the Tumor directly. Instead, it allows the Immune System, the Militia to work as it was designed to work, as it should work, undeceived by the Tumor's deceitful lies. Leronlimab makes it possible for the lymphocytes and White Blood cells to understand that the Tumor is "non-self", that it is in fact an "invader" and that it absolutely must be destroyed.
White Blood Cells were never meant to be Zombies. They were never meant to be deluded by the RANTES chant which the Tumor sings incessantly. No, the Tumor is not supposed to grow inside our bodies. Correct. White Blood Cells are supposed to work for the body, not for the Tumor. All leronlimab does is to allow or cause our Militia to work as they were duly designed to work, as they ought to work, in the way they were meant to work. Leronlimab does not attack the Tumor directly, but by giving the WBCs back their earned authority, leronlimab restores the normal Law and Order, normalcy and health back to the body before it was stolen away by the trickery of the Tumor.
Leronlimab brings back the prior Law and Order before the Tumor's lawlessness ruled the land. Leronlimab re-establishes the Immune System back to its normal activated self. It restores the Killer Cells to again be Killers which through leronlimab's help, exceeds the Tumor's deception.
The Tumor itself is deceived. It is foolishly under the impression that it owns the body. It believes that it has free reign to overtake the entire body. With its deceptive RANTES language, it could do as it pleases. Why? Because RANTES puts the Militia to sleep. RANTES takes a fighting Macrophage and turns it into a Tumor's Slave. However, the Tumor meets its match when leronlimab is introduced; the Tumor loses all of its authority, all of its control immediately is lost when leronlimab confuses the Tumor's language, RANTES. Leronlimab makes it impossible to understand one word the Tumor is saying. Just like in the Tower of Babel, the people could not understand each other and were forced to scatter, the same goes for these WBCs, they no longer could understand the Tumor, so they returned to being who they were before being cast under the Tumor's Trance.
So that's what leronlimab actually does, at least in oncology. It gets rid of the false bio-chemical inter-cellular talk happening within the body. It gets rid of all the gas lighting; the hypocrisy, the lies, the bribes and the blackmail put out by the Tumor. It brings about the real human capacity that is duly incorporated within each of us that is capable of overcoming this Tumor if only the Immune Defensives were not deceived. Leronlimab restores health, but unfortunately could leave a little bit of dirt remaining that might still stain the otherwise washed shirt. Leronlimab does not directly eradicate the Tumor, so therefore, some Tumor could be missed by the WBCs. And these Tumors are virulent; they are determined to survive, even if only one cell is left behind. Yes, leronlimab does bind to the CCR5 receptors on the Tumor's cell surface, but when it does so, it does not induce a direct command to cause that Tumor cell to be put to death. Rather, it marks the Tumor's locale.
However, while leronlimab is on board setting things right in patients plagued with Tumor, Monitoring CTCs and CAMLs throughout this treatment period can clearly depict leronlimab's efficacy in the eradication of these Tumors from the body. The fact that CTC and CAML both decrease significantly with leronlimab treatment is proof positive of leronlimab's efficacy in its ability to eradicate the Tumor. However, the Tumor has much intelligence and much resilience, so not all of it is entirely destroyed. What has recently been discovered is that another survival mechanism of the Tumor, PD-L1 steadily increases in the 30-90 days following the termination of leronlimab, even when starting CPS is low.
Within 30-90 days following the termination of leronlimab, this diagram in RED reveals as compared to the Pre-leronlimab BLUE, that a huge increase in PD-L1 is induced as a result of leronlimab's prior presence and resultant actions. In a last ditch effort to survive, these tiny surviving remnants of the Tumor, which could have been dormant, with the 30-90 day absence of leronlimab, decide to wake up and now put out much more PD-L1 than what they put out prior to leronlimab.
While under current administration and treatment of leronlimab, the remaining shriveled up Tumor and Tumor particles could make attempts at hiding inside the body, going into remission, such that once Tumor, but today left for dead, can somehow Escape the body's Immune recognition. These remnant Tumor cells must remain out of sight, Escaping Immune Detection, until another means to deceive the Immune System is established. Why? Because the tumor also wants to live and does not want to remain in remission ad infinitum. While in remission, the Tumor cells prepare to ramp up their production of PD-L1.
Somehow, those hiding surviving remnants of Tumor are able to overcome leronlimab's RANTES blockade. Leronlimab held them at bay, no longer multiplying, but rather, held them in remission. Despite all the leronlimab that was administered, these remnants of Tumor persisted, however much weakened and reduced they became. These Tumor cells came to the point of realization that RANTES was no longer of any use. Every time RANTES was issued, its communication was ignored because of leronlimab's presence. Therefore, those remnants of Tumor required the ramping up of another language, with which they could make yet another attempt to fight back. They needed a separate language, which had nothing to do with RANTES. They required a more direct language, that spared the Tumor cell specifically.
Tumor was forced to resort to this crafty trick in order to survive. In their time of hiding, while in remission, these dormant Tumor cells further developed and exploited their PD1 axis by expressing more PD-L1 than ever before. If these Tumor cells could still convince the attacking Killer Cells that they were "self", like they used to do when they spoke RANTES, then they would be golden. That's what they thought at least. This crafty trick is exactly what these surviving remnants of Tumor did in order to exit out of their remission. It is through this very trick and also through the misuse of the RANTES language that Tumors steal the "Keys to the Kingdom". This is how Tumors assume "Authority" in the body. This is how they live rent free within our bodily organs.
As to those who did not receive subsequent ICI treatment, those are they who succumbed to the disease. But as to those who did receive subsequent ICI treatment, those are they who are alive today.
Yes, we already have a solution to this hijacked inter-cellular bio-chemical language, PD1 axis. That solution is a PD-1 inhibitor. An ICI or Immune Checkpoint Inhibitor such as Keytruda as discussed in this Link or Opdivo is another one of which there are many. Therefore, our MOA #2 becomes inhibition of the PD1 axis, which is the inter-cellular bio-chemical communication between PD-1 and PD-L1. This takes place directly on the Tumor's Cell surface and it is the last line of defense the Tumor Cell can use to survive. It is the physical recognition of what is "self" and what is "non-self". If you can't tell a Killer Cell that you are "self", then you are "non-self" period, end of story. I wrote the following in Looking On Up:
"I'm thinking MOA #2 has to do with the blockade of another chemokine. Why is MOA #2 necessary? Because MOA #1 doesn't do it alone. It requires MOA #2 to achieve that Vaccine Like Result. So, in order for these two MOAs to synergize with each other, they need to talk to one another. That means they need to speak the same language."
This is the means by which Tumor survives. The Tumor is abnormal human tissue. It owns the human DNA, so it has the means to speak. The Tumor innately knows how to create and manufacture PD-L1 and it put it out in vast amounts to tell every Killer Cell, that it was "self". This caused the Killer Cells to move on to another cell.
This is another language, the PD1 axis, but, more importantly, it is exclusive and independent of the RANTES language. It has nothing to do with RANTES, therefore, it works independent of RANTES. So, this new language, the PD1 axis, distinguishes between "self" and "non-self" and for all the "non-selfers", they are killed outright by the listening WBC and for all the "selfs", they are simply left alone to do their thing.
Combining MOA #1 of RANTES Inhibition and MOA #2 of PD1 axis Inhibition, it all begins with MOA #1 and treatment with leronlimab. Eventually, the Tumor is brought to its knees and under the control by the body's Militia. CTCs and CAMLs should be monitored as should PD-L1 levels. When PD-L1 Expression exceeds a certain threshold, MOA #2 must be initiated by starting a PD-1 inhibitor like Keytruda. Therefore, what leronlimab initially began, Keytruda or another PD-1 blocker finishes.
Results Section of the mTNBC ESMO 5/15/25 Poster
Leronlimab begins the job because Keytruda could not, because the PD1 axis was not even present, at any substantial level at the beginning, see the lower BLUE lines and lower CPS in Figure 4 above. That is what defines the Tumors originally as a "Cold" Non-Responding Tumor . The destruction Leronlimab caused to the Tumor's Micro Environment subsequently induced the development and strengthening of the PD1 axis bio-chemical and intercellular communication channel within the Tumor cell, allowing that cell to communicate with the body's Militia and subsequently come out of remission. Now, with the Tumor at the get-go of utilizing The PD1 axis to convince Killer Cells that it is "self", this is the prime time to initiate a PD-1 Inhibitor in order to achieve 100% eradication of the Tumor, and the full restoration of the body to its original once Tumor free state.
"CytoDyn recently reported that in a small group of metastatic triple-negative breast cancer (mTNBC) patients who received leronlimab at doses of 525 mg or higher and were also treated with any immune checkpoint inhibitor (ICI), 100% (5 out of 5) remain alive as of the latest follow-up. Of these, 80% (4 out of 5) currently have no evidence of disease, while the fifth patient is alive and classified as “stable” by their clinical site. These patients had previously failed a median of two prior lines of metastatic treatment, highlighting the significance of the result. The survival benefit was specifically observed in those who showed a significant increase in PD-L1 expression after leronlimab and then received an ICI."
Conclusion Section of the 5/15 mTNBC ESMO Poster
Figures 4 & 5 of the mTNBC ESMO 5/15/25 Poster
Both mechanisms are necessary. MOA #2 can not go first. It must go second. Leronlimab prepares the Tumor MicroEnvironment for the coming ICI. Both MOAs are necessary to get the job 100% completely done. If the process is stopped at MOA #1, then a Tumor resurgence becomes very possible, because the Tumor could develop the capacity to speak on the PD1 axis PD-L1 which would allow the Tumors to again replicate and even proliferate. The CCR5 blockade no longer would work against that because at this point, the Tumor no longer relies on RANTES to proliferate, rather, it has become a "Hot" type Tumor which now relies on PD-L1 to proliferate, returning to it the ability to outright lie to the Killer Cells, convincing them that the Tumor is "self", so as to ward off their fatal attack and absolute death.
There is this beautiful synergy between our CCR5 blockade and PD-1 blockade. Together, this synergy restores normalcy in the Tumor MicroEnvironment, which is extremely detrimental to the Tumor. This synergy comprised of 2 related but distinct communication blockades restores the Law of the Land; it hands Dominion over the Tumor to leronlimab and to the ICI. If done right, it has the potential to kill cancer entirely. Cancer made a living by mistreating, fooling and deceiving our Immune System, but now, with this Synergistic Development of communication blockades, our Killer Cells can no longer be mistreated. That's why these patients absolutely require Livimmune and why CytoDyn is on the brink of bringing this synergistic solution to the world. In fact, it shall be incorporated into the MSS mCRC Clinical Trial. Thank you kindly Ken. So very much appreciated and respected.
Livimmune is CytoDyn's Brand, and now needs to depict itself as The Brand of course with leronlimab, but also including a PD-1 blocker. The main image of this Brand needs of course to incorporate both leronlimab, CCR5 blockade and a PD-1 blockade. This combination MOA should be represented in an Image or Diagram which becomes CytoDyn's combination MOA and Brand Livimmune. Those of you who are adept at AI Image and Diagram Creation, let's see what you can come up with. Please post your creations.
Compare and Contrast leronlimab with a PD-1 Inhibitor. Both are mono-clonal antibodies that work as bio-chemical inter-cellular communication regulation blockades. One works by the restoration of the Immune System and over time restores health to the body. One works instantaneously, such that at any moment, any failure of that communication channel to properly communication immediately results in swift Tumor Cell death. One blockade works indirectly where as the other blockade works directly. The job can not be started without leronlimab. It is the cause of the transformation from "Cold" to "Hot". Once "Hot", the the ICI can finish the job. In the end, the PD-1 blockade is the finisher while the CCR5 blockade sets the scene and rolls out the red carpet for the ICI to complete the job.
When patients see that Branded Image on the package, they shall know that they have great likelihood of 100% cure of their disease. Regardless of how minimally Responsive their Tumor is originally, leronlimab turns it into a Responsive Hot Tumor, transforming a Cold Tumor into a Hot Tumor, one that is treatable by PD-1 blockade so as to restore health and normalcy to their body.
I wrote the following in Leader Of The Pack late April, 2025 and it stands today.
"Therefore, I think CytoDyn needs to hope for good results with Keytruda concerning mTNBC. Let's hope that the results are better than the results SG got with Keytruda. I think if leronlimab does in fact augment Keytruda's results in mTNBC, then, CytoDyn Oncology Advisory Board needs to determine exactly how it helped Keytruda and through the use of AI Technology, determine how leronlimab could in fact augment Keytruda's results in ALL of their other 30+ Oncology indications.
If leronlimab does in fact help Keytruda in the murine mTNBC study, then, it should tag onto its back, because just as PD-L1 is very much omni-present in the tumor micro-environment, (TME), so CCR5 is ubiquitous. CCR5 is virtually omni-present not just in the TME, but in so many other milieus. PD-L1 is ~33% ubiquitous in the TME and leronlimab should be paired with Keytruda for that simple reason; certainly, if they work well together in the coming murine mTNBC study."
Posted May 18, 2025, 9:54 AM UTC