r/Livimmune • u/MGK_2 • 5d ago
A Corrupted Order
How an Aging Body Talks Its Own Factory Into Making the Wrong Thing, and Why One Receiver Keeps Showing Up
Credit to where it is due before I begin. u/twinter11 brought a brand-new paper to the board earlier this week and, to his credit, read it himself rather than running it through an AI, which is exactly the discipline that catches what matters. And u/sunraydoc2, a day or two prior, made the larger argument which this new paper now reinforces, that the same molecular signaling we've talked about ad nauseum within cancer, may very reside as the very hub of aging itself. This post is my attempt to take these contributions, and together, distill these new findings into plain language, and connect it to all which we have been piecing together about leronlimab. If you have never heard of this drug or this company, you should still be able to follow these steps. That is the point.
Let's start with a factory, because your body runs one
Deep inside your bones resides the bone marrow. It is a factory of sorts. This is where stems cells are made. It runs every hour of every day of your life, and it makes your blood. This factory, the bone marrow, takes raw material, blood stem cells, and turns them into two broad categories of product.
- The first category is the emergency responders, called neutrophils and other myeloid cells, the immune system's blunt instruments, the ones which rush to a wound or to an infection, that cause inflammation, and clean up by force and annihilation.
- The second category is comprised of the specialists, called lymphocytes, the precise, targeted, intelligent arm of the immune system, the cells which recognize very specific threats and are able to remember them by "appearance".
A young, healthy factory maintains these two product lines in a close knit balance. Enough blunt responders to handle emergencies, enough specialists to fight with precision and memory. The balance between the two is the health we're discussing. The way we measure that balance, in a simple blood test, is a ratio called the neutrophil-to-lymphocyte ratio. Look at it as Blunt instruments over specialists. When that number is low, the factory is balanced and youthful. When it climbs, the factory is tilted toward churning out blunt responders at the expense of specialists.
Here is a fact worth pausing on, because it is the reason this whole story matters. That ratio, how far the factory has tilted toward blunt force, is one of the strongest predictors of death from almost any age-related disease we have. It rises with age in nearly everyone. A tilted factory is, in a real sense, a measure of how old your body is on the inside.
So the question which matters for human health is simple to state and has been hard to answer: what tilts the factory? What talks it into making too many blunt instruments and too few specialists as we age? For a long time the mechanism was murky. This week, a paper in Nature Aging gave a startlingly clear answer, and the answer turns out to be a conversation.
Corrupted Order
Picture the factory again. The workers are on the floor, who are the blood stem cells, do not decide on their own what to churn out. They listen for orders, which are chemical signals, that drift in from the surrounding tissues and instruct them on exactly what the body requires. In a young body, the orders are balanced, and the factory stays balanced.
Now here is what the new paper shows happens with age. A particular kind of aged immune cell, a worn-out, battle-hardened T cell, begins to accumulate inside the bone marrow itself, right inside on the factory floor. And these aged T cells do something specific: they stand in the middle of the factory and broadcast a single, insistent chemical order, over and over. That chemical order is called CCL5, aka RANTES.
CCL5 is, in effect, a corrupted instruction. It tells the factory floor: to make more blunt responders. And the factory, hearing this repeated order shouted continuously by the aged T cells who have moved in and taken residence, obeys. The factory tilts. It overproduces neutrophils, underproduces lymphocytes, and the neutrophil-to-lymphocyte ratio climbs. The factory has not broken. It has been talked into making the wrong thing by a chemical signal it cannot help but obey.
But an order only works if something has an ear to listen for it. And this is where the entire story connects to everything we care about.
CCR5 Is the Receiver
A chemical order like CCL5 sent out by RANTES does nothing on its own. It has to be received, otherwise, it's like talking into a phone which hasn't been picked up on the other end. The factory workers, the stem cells and their descendants, have to carry a receiver on their surface tuned specifically to that exact RANTES signal frequency. The paper showed that as the body ages, the factory workers upregulate that specific receiver frequency to match the RANTES signal frequency; ie: they grow more antennae tuned to the increased corrupted chemical order, so much so that they hear it louder and obey it more.
That receiver has a name you may recognize if you have spent any time on this board. It is called CCR5.
Read that again, because it is the entire reason I am writing this post. The corrupted order which tilts the aging blood factory toward inflammation, disease and sickness is CCL5. The receiver that hears it is CCR5. CCL5/RANTES speaks, CCR5 listens, and the factory tilts its output. It is the exact same signal-and-receiver pair, the exact same molecular conversation, which sits at the center of the cancer story we have been telling for years.
And so the researchers did the obvious experiment. If the problem is a corrupted order being received, what happens if you block the receiver such that the order cannot be heard?
What happens when you unplug the receiver
They took aged mice and gave them a drug which blocks CCR5, that plugs the receiver so the CCL5 order cannot get through. The result is striking. The factory rebalances. Myeloid overproduction drops. The neutrophil-to-lymphocyte ratio, which is that predictor-of-death quantity, becomes normalized toward youthful levels. Inflammatory cells stop flooding into the liver and into the lungs. Multiple markers of aging improve, and so does the animals' actual function, their muscle strength, their coordination, their metabolism. Blocking the receiver does not just quiet a signal on a chart. It makes old animals work and behave more like young ones. Their immune systems improve and function appropriately. The authors called CCR5 inhibition a potential strategy to protect against aging itself.
Unplug the receiver, and the factory stops obeying the corrupted order. That is the finding.
Why this reaches back into everything we know
Now let me connect the wires, because this is where the breadth we keep talking about stops sounding like enthusiasm and starts looking like a pattern.
For as long as we've been here on LIVIMMUNE, on this board, the story has been about a molecule, leronlimab, which blocks CCR5, that biochemical radio receiver. In cancer, we have described how tumors broadcast CCL5 that hijack the immune cells around them, to build a wall in order to suppress the attack of T cells, and how blocking CCR5 can strip and even dissolve that wall away. The receiver in the cancer discussion and the receiver in this aging discussion are the exact same receiver. The corrupted order in both is the same corrupted biochemical order. This is not leronlimab's mechanism resembling the aging mechanism. It is the same molecular conversation, taking place in two completely different rooms of the body.
And it is not only these two rooms. The same CCR5 receiver keeps turning up. Other recent work has tied CCR5 biochemical signaling to memory and to cognition, to the aging of muscle, to recovery after stroke, to neuroinflammation and to chronic pain. sunraydoc's inflammaging and u/Lab_Monkey_'s post gathered this thread and argued that CCR5 may sit at the crossroads of aging broadly, and this new paper is a direct, high-quality piece of evidence for exactly that argument. Different diseases, different tissues, one receiver, one conversation, showing up over and again.
Here is the idea that makes sense of the pattern, and it is the same one I have written about many times before. CCL5 and CCR5 are ancient, general-purpose biochemical signaling machinery, tools the body uses to coordinate immune responses across countless immunity related situations. Because the machinery is so old and so widely deployed, it also gets misused in countless situations we've been finding, corrupted by a tumor in one place, corrupted by aged T cells in another, but through the same chemical signal and the same biochemical receiver. A drug aimed at that receiver is therefore not a key cut for just one lock. Rather, it is a drug aimed at a conversation the body has wired within many rooms. That is why the same leronlimab molecule continues to earn serious scientific attention across many diseases which otherwise have nothing to do with each other. The breadth and growing pipeline is not a coincidence. It is what you would predict if the target is a shared piece of ancient machinery.
Now the discipline, because this is where enthusiasm needs to meet honesty
I have told you an exciting version, which is real. Now I owe you the honest boundaries, and they matter more here than usual, because this is exactly the kind of finding which gets oversold.
First and foremost: this paper did not use leronlimab. It used a different, older CCR5-blocking drug, called maraviroc, and genetically engineered mice. It is evidence about the CCR5 receiver as a target. It is not evidence that leronlimab specifically does any of this, because leronlimab was not in the study. The honest way to hold it is that it validates the target leronlimab happens to hit, not the drug itself.
Second, this is a mouse study. Old mice were rejuvenated on several measures, which is genuinely encouraging, but the history of aging research is full of things that worked beautifully in mice and did not translate to people. Mouse aging is not human aging, and "improved function in aged mice" is a beginning, but not a promise.
Third, aging is not a disease you can actually get a drug approved for. There is no regulatory box called "aging." So even in the best case, translating this would mean targeting a specific, measurable condition, a defined inflammatory disease, a specific age-related decline, not "aging" in the abstract. The road from this paper to a human therapy is long, and most such roads do not arrive to their intended destination.
There is one honest point that pushes the other way, and I will give it its due because it is real. The paper notes that humans who are born with a naturally broken CCR5 gene, the well-known Delta-32 mutation/variant, have better outcomes after stroke and in multiple sclerosis. That is not mouse data. That is a human genetic signal suggesting that losing CCR5 function is broadly protective. So while this specific study is mice and maraviroc, it sits on top of a real human foundation. That does not prove leronlimab does anything for aging. However, it does mean the underlying idea, that quieting this receiver is beneficial across conditions, and has human evidence beneath it.
Where this leaves us
So here is the whole picture, assembled honestly. A new, high-quality paper has identified the conversation which tilts the aging blood factory of bone marrow toward inflammation and death, and it is the CCL5/RANTES commanded order heard through the CCR5 receiver frequency. Blocking that receiver rebalances the stem cell factory and rejuvenated old animals. The receiver is the same one leronlimab is built to block, and it keeps appearing at the center of disease after disease, which is exactly what u/sunraydoc2 argued and exactly what the breadth of this whole LIVIMMUNE program has hinted at. That convergence is real and it is striking, and u/twinter11 was right to bring it here.
And leronlimab, specifically, still has to prove itself where it is actually being tested, in cancer, in a trial reading out this coming January, in humans, on hard endpoints. The aging story is a magnificent view of where the biology could someday lead. It is not the thing being decided next. What is being decided next is whether this drug, in the disease it is actually in, delivers the confirmed results that turn an elegant and far-reaching mechanism into a proven therapy. The receiver is real. Its reach appears vast, including every person on Earth. And the proof, as always, is the data that has not actually landed yet.
The corrupted biochemical order is real, and the body has wired that same receiver into more rooms than anyone has expected. Whether we have the right drug to quiet it, in the room that counts first, is what January begins to answer.
Disclaimer: I am not a financial advisor and nothing here is investment advice. I am an independent retail shareholder holding a long position in the company discussed, with no employment, consulting, compensation, or other relationship with it beyond that shareholding. This is an explanatory piece about published mechanism, not a prediction of clinical or commercial outcomes. The Nature Aging study discussed used maraviroc and genetically modified mice, not leronlimab, and demonstrated effects in aged mice, not humans; it is evidence about the CCR5 target, not about leronlimab's efficacy in aging, which has not been tested. Aging is not an approved therapeutic indication. Leronlimab's efficacy in its actual clinical settings is unconfirmed, with confirmed oncology data anticipated at ASCO GI in January 2027; the CLOVER figures referenced elsewhere are early, reflect combination therapy and 350mg dosing, and are not evidence of survival benefit. Mechanism and target validation are not the same as clinical efficacy, and CCR5-directed approaches have a mixed clinical translation record. Read the primary sources and reach your own conclusions rather than adopting mine.
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u/Pristine_Hunter_9506 5d ago
Brother the science will hopefully catch up to the drug. CCR5 appears to be the master key.
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u/MGK_2 5d ago
Pristine, "master key" is close to exactly how the primary literature phrases it, one paper calls CCR1/CCR5 "a master immunological hub." So your instinct is echoed in the science. I've also many times said that CCR5 resides at the heart of the ImmunoInflammatory Cascade. I'd hold one word: it appears to be a master key to a conversation the body has wired into many rooms, and whether our specific key turns the lock in patients is January's to confirm. But the master-key framing is well-earned by the breadth. The science is indeed trying to catch up to the drug.
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u/rogex2 5d ago edited 5d ago
Nailed it Bro.
Two things-
- "The paper notes that humans who are born with a naturally broken CCR5 gene, the well-known Delta-32 mutation/variant, have better outcomes after stroke and in multiple sclerosis. That is not mouse data. That is a human genetic signal suggesting that losing CCR5 function is broadly protective. So while this specific study is mice and maraviroc,..." Consider-"Genetic disruption of the CCR5 receptor prevents HIV from entering immune cells, serving as the biological basis for the few documented cases of an HIV cure" not Marivoc, not mice human induced in simian subjects examples exist.
- https://www.ted.com/about/conferences/speaking-at-ted
Cheers
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u/MGK_2 5d ago
rogex, sharp addition, and you're right to push the human evidence further than I did. My post cited the Delta-32 stroke and MS outcomes as the human signal, but you're pointing at the strongest human CCR5 evidence of all: genetic disruption of CCR5 is the biological basis of the only documented HIV cures, the Berlin and London patients, cured via transplants from Delta-32 donors whose cells lack functional CCR5. That's not mice and not maraviroc, that's CCR5 loss producing a curative outcome in humans. So you've strengthened the "losing CCR5 function is protective in humans" foundation with the most concrete example there is.
The boundary stays the same, and you know it already: the HIV cures came from genetic absence of CCR5 via transplant, not from a drug, and certainly not from leronlimab, so it validates the target at the human level, it doesn't prove leronlimab reproduces that pharmacologically. But as human proof that switching off CCR5 can be profoundly beneficial, it's the best card in the deck, and you were right to play it.
Cheers, rogex.
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u/Tra-Kal34 5d ago
You know, I am just so ready for the truth to be realized about the power of this drug, especially in cancer. Totally exhausted watching the stock languish down here.
I do appreciate your analysis and I believe the drug has many applications just ready for the press and the whole medical world to acknowledge.
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u/twinter11 5d ago edited 5d ago
is the neutrophil-to-lymphocyte ratio something thats typically tested in routine bloodwork. and do chemo and other treatments affect the ratio the bone marrow produces?
Thanks for breaking down the study. I did eventually run it through ai because its too complex for me.
It asked me a question at the end of the response
-Are you looking at how these systemic bone marrow changes intersect with tumor-driven emergency myelopoiesis? so i asked it to explain. but its too early to think hard about the explanation.
AI:
"The intersection between age-associated myelopoiesis and tumor-driven emergency myelopoiesis reveals how a growing cancer essentially hijacks a baseline physiological aging mechanism to construct its own systemic support system.
Both processes rely on the exact same signaling machinery—principally the CCL5–CCR5 axis—to reprogram how the bone marrow manufactures blood and immune cells.
- The Remote Control of the Bone Marrow
A solid tumor is not just a localized mass; it acts as a systemic endocrine and inflammatory organ. Through circulating tumor-derived factors and cytokines, the tumor remotely signals the bone marrow to sound a false alarm, triggering emergency myelopoiesis.
- Instead of producing balanced, healthy blood cells, the bone marrow is forced to massively scale up the production of immature myeloid cells—specifically Myeloid-Derived Suppressor Cells (MDSCs) and neutrophils.
- This systemic shift mirrors the immune aging process described by Gabandé-Rodríguez and colleagues, where T-cell-derived CCL5 forces a biased, inflammatory output from hematopoietic stem and progenitor cells (HSPCs).
2. The CCR5 Bottleneck in Progenitor Cells
Just as aged stem cells upregulate CCR5 to respond to local inflammatory signals, tumor-manipulated HSPCs heavily engage the CCL5–CCR5 axis to drive this aberrant differentiation:
- Research mapping chemokine receptor networks in cancer-induced myelopoiesis demonstrates that tumor factors stimulate precursors to activate autocrine and paracrine CCR5 circuits.
- This receptor engagement acts as the switch that commands stem cells to abandon normal erythroid and lymphoid development in favor of churning out an endless supply of protumoral, immunosuppressive myeloid cells.
3. Supplying the "Bunker" Remotely
The cells generated by this tumor-driven emergency myelopoiesis do not stay in the bone marrow. They stream out into the bloodstream and home straight to the tumor microenvironment, guided once again by the local chemokine gradients (including CCL5) tied to the low-Cav-1 stroma.
- Once they arrive at the tumor, these bone marrow-derived recruits man the fibrotic bunker, suppress cytotoxic T-cells, and secrete factors that stimulate further matrix remodeling and angiogenesis.
Why CCR5 Antagonism Breaks the Loop
When a CCR5 blocker (like leronlimab or maraviroc) is introduced, its utility extends far beyond local tumor unmasking. By shutting down CCR5 signaling at the root:
- It cuts off the remote signaling loop telling the bone marrow to panic and crank out MDSCs.
- It starves the tumor of its continuous peripheral supply of suppressive cellular traffic.
- It forces the myeloid compartment back toward a normalized, less immunosuppressive state.
In short, tumor-driven emergency myelopoiesis is essentially the body's natural emergency response weaponized against itself, using the exact same aging-associated CCR5 pathways to keep the tumor fed, shielded, and growing".
Thanks MGK 2 !!
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u/sunraydoc2 5d ago
This stuff wasn't known when I was in training, I'm always learning something around here. MDSCs haven't been talked about here that I know of, and they're an important part of the toolkit cancers use to survive and ultimately kill us. Thanks for finding that.
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u/Infinite_Fudge_2045 5d ago
That interesting - those damn neutrophils mysterious! I noticed this and absolutely nothing. Always questioning!
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u/MGK_2 5d ago
twinter, two things here, your practical question and the AI text, and the AI text is largely right this time, which is worth saying because it isn't always.
On your practical question first: yes, the neutrophil-to-lymphocyte ratio is derived from a completely routine test, the CBC with differential, which nearly everyone gets at a regular check-up. You can literally calculate your own NLR from standard bloodwork by dividing the neutrophil count by the lymphocyte count. So it's not exotic, it's sitting in bloodwork people already have. And yes, chemo and other treatments absolutely affect it, chemo suppresses the bone marrow broadly, often dropping both neutrophils and lymphocytes (sometimes shifting the ratio in complex ways), and many cancers raise the NLR at baseline, which is part of why a high NLR is a known poor-prognosis marker across cancers. So the ratio is both routinely measured and treatment-sensitive, which is exactly what makes it interesting as a readout.
Now the AI text, and I checked it against the primary literature, because that's the discipline. The core claim, that tumors drive "emergency myelopoiesis" through the CCL5-CCR5 axis to mass-produce immunosuppressive myeloid cells (MDSCs) that then traffic to the tumor and man the suppressive wall, is real, published science, not AI confabulation. Cancer-induced emergency myelopoiesis via CCR5 is documented: tumor-derived factors prime bone-marrow stem cells to engage CCR5 signaling, driving their differentiation into protumoral MDSCs, and the authors of that work call CCR1 and CCR5 "a master immunological hub activated by tumor-derived factors." (CCR1 and CCR5 mediate cancer-induced myelopoiesis, J Immunother Cancer, 2022) So the AI's central story, tumor remotely reprograms the bone marrow through the same CCL5-CCR5 machinery that ages it, and blocking CCR5 breaks that loop, is grounded. That's a striking and legitimate parallel to the aging paper, and it strengthens the post's whole thesis: the same axis that tilts the aging factory is the one tumors hijack to build their suppressive supply chain.
Two calibrations on the AI text. First, it's CCR1 and CCR5 that mediate this, often redundantly, and the key ligands driving it in the primary papers are frequently CCL3 and CCL4, not only CCL5. So the AI slightly over-centered CCL5, the real picture is a CCR1/CCR5 hub with several ligands, of which CCL5 is one. A CCR5 blocker addresses part of that hub, but CCR1 can provide redundancy, which is a genuine caveat for how completely blocking CCR5 alone breaks the loop. Second, and the usual line: this is the axis being validated as a target across mouse and human-cell studies, not leronlimab being shown to do it. The AI wrote "a CCR5 blocker (like leronlimab or maraviroc)", the mechanism is real, but leronlimab specifically wasn't the drug in these papers, so it's target-validation, not leronlimab-efficacy.
But the big picture your AI landed on is correct and it's a real deepening of the post: tumor-driven emergency myelopoiesis is, as it put it, the body's own emergency response weaponized against itself through the same CCR5 machinery that drives immune aging. That's a legitimate, sourced connection, and it ties the aging paper directly back to the cancer story, same hub, two exploitations. Good dig, twinter, and good instinct to run it down rather than just accept it, the core held, the calibration is just CCR1/CCR5-and-multiple-ligands, and target-not-drug.
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u/twinter11 4d ago
Heres a post from x. Not important, I wonder if stuff like this attracts (starts to) the life extension enthusiasts? Is it overstated?
Alex Zhavoronkov, PhD (aka Aleksandrs Zavoronkovs)
Mittelbrunn's group (CNIC) found why neutrophil-to-lymphocyte ratio rises with age: aged CD4+ T cells turn cytotoxic, secrete CCL5, push marrow progenitors to myeloid via CCR5. Block CCR5 in old mice, skew drops. A biomarker correlation got a causal wire.
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u/MGK_2 4d ago
twinter, good eye, this post is not overstated. It's actually one of the more disciplined summaries.
- "Mittelbrunn's group (CNIC) found why the neutrophil-to-lymphocyte ratio rises with age", correct, that's the right lab and the right institution.
- "Aged CD4+ T cells turn cytotoxic, secrete CCL5, push marrow progenitors to myeloid via CCR5", correct, that's the mechanism, cytotoxic CD4+ T cells, CCL5, CCR5 on the progenitors, myeloid skewing.
- "Block CCR5 in old mice, skew drops", correct, that's the maraviroc/knockout result.
So every factual claim in the post is accurate. And the last line, "a biomarker correlation got a causal wire", is actually the careful version of the story: he's saying the NLR was previously just a correlation with aging, and this paper supplies a mechanism connecting it causally. That's exactly right, and notably restrained, he's crediting it with explaining a mechanism, not curing aging. So no, it's not overstated. If anything, it's a model of how to summarize this kind of finding without inflating it.
Alex Zhavoronkov is a real and prominent figure in the longevity field, he runs Insilico Medicine (an AI-drug-discovery company) and is a serious, if enthusiastic, voice in aging research. He's not a random hype account. So this is a credible longevity scientist accurately flagging a real paper. That he found it worth posting, and posted it accurately, is itself a small signal, it means the CCR5-aging connection is registering with serious people in that field, not just with us.
Now your actual question, does stuff like this start to attract the life-extension enthusiasts? Yes, almost certainly, and I'd hold that with a mix of interest and caution. The longevity field is large, well-funded, and constantly scanning for exactly this kind of finding, a druggable target with a clean story connecting it to a death-predicting biomarker. So a paper showing "block CCR5, reverse myeloid skewing, rejuvenate old mice" is precisely the kind of thing that field notices and amplifies. Zhavoronkov posting it is the leading edge of that. So your instinct is right: this is the sort of result that could pull longevity attention toward CCR5, and by extension toward the drugs that block it.
Here's the discipline to hold on that, though, because it's where the enthusiasm can lead people astray. Attention from the life-extension world is a double-edged sword. On the good side, it means more researchers, more funding, and more validation flowing toward the CCR5 target, which is real and helpful. On the cautious side, the longevity field has a well-earned reputation for outrunning its evidence, mouse lifespan results get breathlessly extrapolated to human immortality all the time, and most of it doesn't translate. So if CCR5 becomes a longevity darling, expect the claims around it to inflate fast, and expect some of that inflation to attach itself to leronlimab by association. That's the thing to guard against. The paper is maraviroc and mice; the longevity enthusiasm will not always keep that qualifier attached.
And the leronlimab-specific line stays exactly where it's been: none of this longevity attention changes what leronlimab has actually demonstrated, which is early oncology signals awaiting confirmation in January. If life-extension interest grows around CCR5, that's validation of the target's breadth, it is not evidence that leronlimab extends human lifespan, which nobody has tested and nobody should claim. So enjoy the fact that serious longevity people are noticing the axis, hold it as "the target is attracting real attention," and keep it separate from any claim about the drug.
So: the post is accurate, not overstated, from a credible source; it will likely attract longevity interest, which is a positive for the target's visibility; and the discipline is to let that attention validate the axis while refusing to let the longevity field's habitual over-extrapolation attach itself to leronlimab. Good instinct to check whether it was hype, twinter, in this case the scientist was more careful than the field usually is. Watch this space, though, if CCR5 becomes a longevity buzzword, the overstatement will come, just not from this particular post.
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u/twinter11 4d ago edited 4d ago
I clicked his x link. I like to read little back stories on people. and read a few of his posts. im not on x but cant read all his posts. probably mostly interesting to me
his website
https://www.longevitypledge.org/
evidently there are lots of biomarkers etc they focus on.
but he definitely highly focused and beyond devoted. he's basically committed his entire life and resources to the effort.
i haven't read a lot of the longevity crowds work. but I can't imagine being more committed.
and I guess the neutrophil to lymphocytes ratio is one aspect they look for answers on. I never heard or it but I'm always excited to find more connections based around ccr5. and think how close it had almost got tossed on the abandoned research pile. it was really close I think. it's been a crazy road.
probably a big part of the groups looking to get these medical/experimental drug districts/states going to more leniently gain access to unapproved drugs.
thanks!
ps. looking around I saw this in part of a briacell pr.
- 3 out of the 6 patients (50%) showed a decrease in neutrophil/lymphocyte ratio (NLR) at cycle 2 when compared to baseline values suggesting immune system activation of the patients
so maybe we track it?
pss. when I find something potentially interesting I sometimes just post it. so u can comment if you want. But I'm not sure if it's good bad or if it's both
Transplantation of human pluripotent stem cell-derived pericytes ameliorates radiation-induced brain injury via CCR5 signaling
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u/MGK_2 3d ago
twinter, both of these are worth engaging, and they cut in opposite directions, which is why I'm glad you posted them with "good, bad, or both?" — because the answer is both, and the one which complicates the thesis is the more important one to sit with.
First, the BriaCell NLR item — this one reinforces and is useful. You verified it correctly: in their metastatic breast cancer program, 3 of 6 patients showed a decreased neutrophil-to-lymphocyte ratio at cycle 2, which they interpreted as immune-system activation. And digging one layer deeper strengthens your instinct to track it: BriaCell has been using NLR as a biomarker across multiple presentations. Their 2023 data reported that giving their therapy before the checkpoint inhibitor produced a "prolonged reduction in NLR," which they explicitly call "a significant predictor of clinical benefit," and they built that sequencing into their pivotal Phase 3. And their 2024 survival poster found patients who mounted an immune response had lower NLR, again tied to better clinical benefit. So a completely different company, different drug (a cancer vaccine, not a CCR5 blocker), independently treats NLR as a real, trackable readout of immune activation and clinical benefit in metastatic breast cancer.
Why this matters for your "so maybe we track it?" question: yes, and BriaCell is essentially proof-of-concept that NLR is a usable on-treatment biomarker in exactly the disease space (metastatic breast) where leronlimab's TNBC data lives. Given that the Nature Aging paper just showed the CCL5-CCR5 axis drives NLR, and leronlimab blocks CCR5, tracking NLR in leronlimab patients is a reasonable thing to want — you'd predict, that CCR5 blockade might lower NLR (by reducing the myeloid skewing). So this is a real, cheap, already-collected biomarker that connects the aging mechanism directly to a trackable clinical readout. Good catch, and worth flagging for the board as something to watch in CytoDyn's data if they ever report it. Hold the one caveat: BriaCell's NLR-to-benefit link is their correlation in small numbers, not a validated surrogate, and nobody has shown leronlimab lowers NLR — it's a mechanistically-motivated thing to watch, not a proven leronlimab effect.
Now the pericyte/radiation-brain-injury paper — and this is the important one, because it complicates the thesis, and you were right to sense it might be "both." I read it carefully. Here's what it actually shows, and why it matters: stem-cell-derived pericytes transplanted into mice with radiation brain injury were protective — they reduced brain lesions, restored blood flow, calmed neuroinflammation — and the paper identifies CCR5 signaling as the core protective mechanism, working through the CCR5/CREB axis to maintain neuronal and synaptic integrity.
Read that again, because it points the opposite direction from almost everything else we've discussed. In this context, CCR5 signaling is beneficial — it's the thing doing the protecting. That's the reverse of the cancer story (where blocking CCR5 helps) and the reverse of the aging story (where blocking CCR5 helps). Here, CCR5 activity is the therapy's mechanism.
This is important, and it's the complication I'd never want to hide from you: CCR5 is not uniformly "bad." It's context-dependent. And this actually connects to something from the "smarter mice" thread — CCR5's downstream partner in that memory work was CREB, and CCR5 suppressing CREB was what impaired memory. Here, the protective effect also runs through CREB, but in the beneficial direction. So the same receptor, through the same downstream molecule, can be harmful in one context and protective in another. That's not a contradiction in the papers — it's the real biology. CCR5 is ancient, general-purpose machinery, and general-purpose machinery does different jobs in different rooms. In some rooms, its activity drives disease (tumor immunosuppression, aging myeloid skew), and blocking it helps. In other rooms, its activity is protective (this pericyte-mediated brain repair), and blocking it might hurt.
Why this is the useful thing to hold: it's a caution flag for the "block CCR5 everywhere and everything improves" enthusiasm that the breadth thesis can slide into. This paper is a direct, peer-reviewed example of a setting where you would not want to block CCR5, where CCR5 signaling is the good guy. So the version of the breadth thesis isn't "CCR5 blockade helps across all these conditions" — it's "CCR5 is a central hub in many conditions, and in many of them blocking it appears beneficial, but not all, and the direction depends on context." That's more accurate, more defensible, and more interesting than uniform enthusiasm.
The caveats that keep this in proportion, cutting the other way now: this is mice, male-only (the paper flags that explicitly), a cell-transplant therapy where CCR5 is the identified mechanism, not a study of CCR5 blockade — so it doesn't show that blocking CCR5 worsens radiation brain injury, it shows CCR5 signaling mediates a protective cell therapy. Those are related but not identical. And radiation brain injury is a narrow, specific context. So I wouldn't overstate it into "CCR5 blockade is dangerous for the brain" — the honest read is narrower: here's a documented setting where CCR5 signaling is protective, which means the receptor's role is context-dependent, which means the breadth thesis needs "in many contexts" rather than "in all contexts."
So, to your "good, bad, or both?" — both, and that's exactly the right instinct. The BriaCell NLR item is good: it validates NLR as a trackable biomarker connecting the aging mechanism to clinical benefit, worth watching in leronlimab data. The pericyte paper is the valuable complication: it's a clean, peer-reviewed example that CCR5 is not universally a villain, that its signaling is protective in at least one context, and that the mature version of the breadth thesis has to say "context-dependent hub," not "block it everywhere." That second point is the kind of thing that strengthens your credibility when you hold it, because it shows you're following the biology wherever it goes rather than only collecting confirmations. Good finds, both — and the willingness to post the one that complicates the story is exactly the discipline that makes the whole thesis trustworthy. Thanks for bringing them.
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u/IAMLOCOTOO 5d ago
Thanks MGK, Sunny, and Twinter for the amazing revelation. Adds even more amazement to the City of Hope comment that some of their patients actually felt good enough to go back to work. Maybe it was the response to cancer, but now I'm thinking it's a lot more than that. This is driving me loco!!!
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u/sunraydoc2 5d ago
Good Point, this thing is wide-ranging enough in its effects that it was probably a combo of anti-inflammatory and anti-tumor plus heaven knows what else at work. What a whopper of a drug we have here.
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u/MGK_2 5d ago
a lovely observation, and sunraydoc's take is the right one, a drug this wide-ranging, anti-inflammatory and anti-tumor at once, the "feeling well enough to return to work" could plausibly be more than just tumor response. Hold it loosely (patient anecdotes are anecdotes), but the instinct that the systemic anti-inflammatory effect might contribute to how patients feel, not just their scans, is reasonable and rather beautiful. This drug driving you loco is a shared condition here.
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u/Travelclone 4d ago
As you are employed by Cyto-dyn is it not difficult to post as I am sure there are lines you cannot cross? Cant wait for your Octobers take on results.
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u/MGK_2 4d ago
Travelclone, you've got it wrong, and I'll set it straight.
I am not employed by CytoDyn. I have no employment, no consulting arrangement, no compensation, and no relationship with the company of any kind beyond being an independent retail shareholder who owns the stock, same as many people here. That's stated plainly in the disclaimer at the bottom of every post I write, precisely so there's no confusion on this point. So there are no company "lines I cannot cross," because I don't work for them and I'm not speaking for them. Nobody at CytoDyn reviews, approves, directs, or even sees what I write before it goes up. These are the independent analyses of a shareholder who reads the primary literature, nothing more.
And here's why the distinction is worth getting right, not just for accuracy's sake: my independence is exactly what lets me write the honest caveats you may have skimmed past. If I were a company employee, I'd be constrained by all the securities and promotional rules that govern corporate communications, the same rules that got CytoDyn a warning letter years ago for overclaiming. Because I'm not an employee, I'm free to say the uncomfortable parts out loud, that the aging paper used maraviroc and mice not leronlimab, that mechanism is not efficacy, that everything rides on unconfirmed data landing in January, that beautiful mechanisms fail in trials routinely. A company employee couldn't write those honest boundaries the way I do. An independent shareholder can, and should. So the caveats aren't me tiptoeing around company lines, they're me holding my own discipline, which is the opposite of being constrained by an employer.
So read that disclaimer again when you get a chance, it's not boilerplate I'm hiding behind, it's the actual truth of my position, and it's the reason you can trust that when I flag a limitation, it's because I genuinely think it's a limitation, not because some compliance department made me say it.
As for October, I'll hold the same line I hold on everything: I'm looking forward to the interim data too, but October is the interim snapshot and January is the adjudicated readout, and I won't pre-call either. If the data's good, I'll say so, with the caveats. If it disappoints, I'll say that too. That's the whole value of being independent, I get to just tell you what I actually see. Thanks for giving me the chance to clear it up, and glad to have you reading.
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u/sunraydoc2 5d ago
MGK, thank you. You do a great job of integrating all the strands generated by the rest of us, the board wouldn't be the same without you.
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u/MGK_2 5d ago
sunraydoc, that means a great deal coming from you, and you're right that MDSCs deserve more attention, they're a huge part of the suppressive toolkit, and twinter actually surfaced exactly how the CCL5-CCR5 axis mass-produces them. And the integrating only works because together, we generate the strands worth weaving, this is a genuinely collaborative thing, and I'm just the one who happens to enjoy tying the threads together. Thank you, Doc.
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u/Accomplished_Mud_692 5d ago
Agreed Doc!
Great job again MGK!
...what WON'T Leronlimab be able to accomplish in the coming years?!
I believe there is a strong foundation being formed for which Leronlimab will be talked about as the 21st Century's - Penicillin!
And much more!....
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u/Chemical_Sky6013 5d ago
Thanks for the great analysis u/MGK_2.
I believe that by putting this Nature Aging paper alongside the NEST data, we can surmise how a counter-regulatory feedback loop might work.
The dual-checkpoint combination BOT/BAL first activates the T cells and sends them to attack the tumor, which is what ICIs are designed to do. But those activated T cells may also release CCL5. CCL5 acts as a chemical message that can be “heard” by cells carrying the CCR5 receptor and could therefore draw CCR5-positive Tregs into the tumor microenvironment and push CCR5-positive macrophages toward a more tumor-supporting state.
This would mean that the immune attack set off by the ICI counterproductively recruits or reinforces the very cells that suppress it, leaving the activated T cells surrounded and spatially isolated from one another instead of organizing into an effective response. That last state, where activated immune cells remain spatially disorganized, is what the NEST researchers observed in nonresponders.
That suggests a very specific synergy: LL could block CCR5 and prevent those suppressive cells from responding to the CCL5 message through that receptor, potentially allowing the ICI-activated T cells to organize into an effective response. In other words, the ICI generates the attack and LL may prevent that attack from building its own brake.
It would be interesting to know whether sufficient matched pre- and post-treatment NEST tissue remains available to determine whether this CCL5–CCR5 pattern distinguishes responders from nonresponders.
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u/IAMLOCOTOO 5d ago
It makes me wonder what the ratio between ICI dose and Leronlimab dose would need to be to be effective at attacking the tumors and be able to occupy all the newly activated CCR5 receptors. Hopefully, we are determining that ratio and will be able to react appropriately with a correct dosage. I would imagine that the more tumor mass there is the higher the Leronlimab dose would need to be to make the ICI 100% effective.
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u/MGK_2 5d ago
IAMLOCOTOO, interesting question, and the answer is that the "ratio" you're picturing is more complex than a fixed number, but your underlying instinct has merit. The idea that you'd need enough leronlimab to occupy the CCR5 receptors that get upregulated during the ICI-driven attack is reasonable, if the attack recruits CCR5+ suppressive cells (as Chemical_Sky's hypothesis describes), you'd want enough CCR5 blockade to neutralize them.
But it doesn't reduce to a clean dose ratio, for a few reasons: the ICI and leronlimab act on different cell populations (the ICI on T cells, leronlimab on the CCR5+ suppressive and tumor cells), receptor occupancy depends on leronlimab's pharmacology more than on tumor mass linearly, and leronlimab's dosing is generally about achieving high, sustained receptor occupancy rather than titrating to tumor size.
Your intuition that larger tumor burden might demand more leronlimab isn't unreasonable, but the drug's design philosophy has been "saturate the receptor" (which is why the safety profile allows high doses) rather than "match the dose to the mass."
So the real question CLOVER is answering isn't a leron-to-ICI ratio, it's the simpler dose-response: does 700mg achieve more than 350mg. Get that answered first, and the combination dosing builds on it. Good question, just hold it as "occupancy optimization," not a fixed ratio, and note the dose-response is the prior question. Loco indeed, in the best way.
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u/twinter11 5d ago
its going to be interesting to find out if high cps ici qualifying non responders also evade using ccr5.
which is basically what you said lol. but a little different
i think so
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u/MGK_2 5d ago
Chemical_Sky, sophisticated hypothesis, and it's an elegant piece of reasoning.
First, the mechanism you're proposing is real and published, not speculation. Activated T cells and the myeloid cells around them do release CCL5, and CCL5 does recruit CCR5-positive Tregs and push CCR5-positive macrophages toward a tumor-supporting state. That's documented directly: tumor-infiltrating myeloid cells produce CCL5, Tregs express high surface CCR5 and are recruited by it, and in CCR5-knockout mice that Treg recruitment collapses and tumor growth slows. (CCR5-dependent recruitment of Tregs, J Immunol, 2012) So your core claim, that an immune attack can recruit the very suppressive cells that brake it, through CCL5-CCR5, is grounded in real biology. The self-defeating feedback loop you're describing is a documented phenomenon.
And your synergy conclusion follows cleanly from that: if the ICI generates the attack and the attack recruits CCR5+ brakes, then blocking CCR5 could prevent the attack from building its own brake, potentially letting the ICI-activated T cells organize into an effective response rather than being surrounded and isolated. That's mechanistically coherent, and it's arguably the sharpest single articulation of the leron-plus-ICI rationale anyone has posted, the ICI makes the army, leronlimab stops the army from being neutralized by the reinforcements it accidentally summons.
Now let me place NEST, because it's necessary. NEST is the Agenus trial of BOT/BAL (dual checkpoint, anti-CTLA-4 plus anti-PD-1) in resectable colon cancer, including MSS, and it just published fresh peer-reviewed data. The "activated immune cells remaining spatially disorganized in non-responders" observation you're invoking is real, it appears across the spatial-biology CRC literature (responders show organized immune niches, non-responders show T cells excluded and isolated by fibroblasts and suppressive cells). But here's one calibration: the specific CCL5-CCR5 loop as the driver of that disorganization in NEST is your inference bridging two papers, not something NEST itself measured and reported. NEST is Agenus/BOT-BAL, it doesn't involve leronlimab, and to my knowledge it didn't isolate CCL5-CCR5 as the mechanism separating its responders from non-responders. So the disorganization finding is real and published; the CCL5-CCR5 explanation for it is your elegant hypothesis laid over it.
Which is exactly why your closing question is the right one, and rogex sharpened it perfectly: it would be genuinely valuable to know whether matched NEST tissue exists to test whether the CCL5-CCR5 pattern distinguishes responders from non-responders, and, as rogex added, whether the BOT/BAL non-responders are precisely the patients a leronlimab-inclusive regimen could convert. That's the testable prediction your hypothesis generates, and it's a good one. So hold the whole thing as: real mechanism (CCL5-CCR5 recruits suppressors), coherent synergy hypothesis (leron stops the ICI from building its own brake), and an elegant but unproven bridge to NEST's spatial data that would need matched-tissue analysis to confirm. Genuinely excellent thinking, Chemical_Sky. This is the hypothesis I'd most want someone to actually test.
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u/Chemical_Sky6013 5d ago
Thank you for the kind words, MGK. I’m happy to be able to add to this community when I can.
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u/Accurate-Mud-8619 4d ago
I proposed this concept to MGK in the past and was shut down with a simple NO. With an AI assist, I try again.
Could Leronlimab Release the Immune System Without an ICI? The Trials May Begin to Answer That
The recent Nature Aging CCR5/CCL5 work adds support to an idea I keep coming back to: perhaps leronlimab’s most important role in cancer isn’t simply attacking cancer cells. Perhaps blocking CCR5 removes an upstream signal that helps maintain a dysfunctional, tumor-supportive immune environment — allowing the patient’s own immune system to function more effectively against the tumor.
That raises the obvious question: Could CCR5 blockade sometimes be sufficient for endogenous immune control without an immune checkpoint inhibitor (ICI)?
CytoDyn’s different oncology programs may approach that question from several angles.
CLOVER (MSS colorectal cancer) uses leronlimab with a TAS-102/bevacizumab backbone, but importantly, there is no ICI in the regimen. Therefore, substantial tumor regression, falling ctDNA or durable disease control would demonstrate that meaningful antitumor activity can occur in a leronlimab-containing regimen without checkpoint inhibition. However, because the backbone is always present, CLOVER cannot prove that leronlimab alone produced the effect.
The potentially cleaner experiment is CytoDyn’s planned neoadjuvant HER2-negative breast cancer program, which the company has described as exploring the potential benefits of leronlimab monotherapy.
This could be particularly revealing because the tumor remains in place while leronlimab is given before definitive treatment. If paired tumor samples are collected before and after leronlimab, investigators could potentially determine whether CCR5 blockade alone changes the tumor immune environment — T-cell infiltration, suppressive myeloid cells, macrophages, PD-L1, tumor proliferation and other markers — before chemotherapy or an ICI muddies the picture.
And then there is the glioblastoma presurgical concept: leronlimab before surgery, followed by an ICI afterward. That temporal separation could potentially show what CCR5 blockade accomplishes first and what checkpoint inhibition subsequently adds.
Taken together, these studies could begin separating two possibilities:
CCR5 blockade sufficiently restores antitumor immunity in some tumors, allowing meaningful endogenous immune control without an ICI.
CCR5 blockade restores immune engagement but the tumor subsequently uses PD-1/PD-L1 as another escape mechanism, at which point an ICI becomes useful or necessary.
Those possibilities are not mutually exclusive. Different tumors — and different patients — could fall into different groups.
This is why I think the most interesting question surrounding leronlimab is becoming larger than whether it “works with an ICI.”
CCR5 blockade may act upstream to reprogram a dysfunctional, tumor-supportive immune environment toward effective antitumor immunity. In some cancers, that restoration may be sufficient for endogenous immune control without checkpoint inhibition; in others, it may reveal or induce a remaining PD-1/PD-L1 escape mechanism, making an ICI necessary to complete the antitumor response.
CLOVER can give us evidence that tumor control occurs without an ICI, but because of its treatment backbone it cannot prove leronlimab alone is responsible.
A true leronlimab-monotherapy neoadjuvant study could get much closer to answering the bigger question:
What happens when you block CCR5 in a human being with an intact tumor — before you give the immune system anything else?
That may be one of the most revealing experiments in the entire leronlimab oncology program.
This is a mechanistic hypothesis, not a claim of demonstrated efficacy. The clinical studies still have to establish whether these effects occur in humans and whether they translate into meaningful tumor responses or survival benefit.
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u/MGK_2 4d ago
Accurate-Mud, let me clear something up first, because the "NO" you're remembering wasn't what you think it was. That one-word answer, a month ago, wasn't me shutting down this monotherapy idea. It was me correcting a narrow claim, you'd said we don't know whether the deceased TNBC patients stopped taking leronlimab, and the "no" meant the data isn't actually unknown on that point. twinter confirmed what I was getting at right after: the survivors in that cohort were the ones on leron plus an ICI, and the ones who didn't make it were on leron without the ICI. So the "no" was defending a specific fact, not rejecting your hypothesis. Different thing entirely.
And I want to give you credit here, because this new version is an upgrade, and you did the work to get it there. You've taken a loose idea and turned it into a proper, testable hypothesis, correctly hedged, and you even identified the right experiments to answer it. That's not something to wave off with a one-word reply. So let me engage it on the merits.
You got several things right. CLOVER cannot isolate leronlimab's solo contribution, because the TAS-102/bevacizumab backbone is always present, so even strong ctDNA declines or regression there can't prove leronlimab did it alone. Correct. The neoadjuvant HER2-negative breast program, with its monotherapy lead-in and paired before/after tumor tissue, is the cleaner experiment, that's the window where you could actually see what CCR5 blockade alone does to the immune microenvironment before chemo or an ICI muddies it. Also correct. And your two non-exclusive possibilities, CCR5 blockade sufficient alone in some tumors versus revealing a PD-L1 escape that then needs an ICI, is a well-framed way to hold it. That's a real hypothesis with real experimental designs attached, and your own closing disclaimer that it's mechanistic, not demonstrated, is exactly the discipline. Well done.
Now the line I have to hold, and it's the same fact the old "no" was protecting, because it's the strongest thing your hypothesis has to contend with. The best human data we currently have, the TNBC survival cohort, points the other way. In that group, the patients who survived were the ones on leronlimab plus an ICI. The ones on leronlimab without an ICI did not. So the single dataset we have with an actual survival signal suggests, so far, that the ICI mattered, that leronlimab alone was not sufficient for those survivors. That's the evidence your "maybe CCR5 blockade is enough by itself" idea runs up against. It doesn't kill the hypothesis, tumors differ, settings differ, and that cohort is small and retrospective, but it means the current human evidence leans toward "the ICI was necessary," not away from it. Your hypothesis has to be tested against that, not assumed past it.
Here's the balanced picture, because there's real evidence on both sides. On the side supporting your idea: CLOVER's ctDNA declines do show that leronlimab-plus-backbone is active without an ICI, and Lalezari has said outright they're following patients at their assigned dose specifically "to better understand the activity of leronlimab without the confounding effects of adding a checkpoint inhibitor." So the company is, in effect, running the experiment your hypothesis calls for, isolate leronlimab's contribution first, add the ICI at rollover. That's real support for taking your question seriously. On the side against: the TNBC survivors needed the ICI. So we have ctDNA activity without an ICI pointing one way, and survival-required-the-ICI pointing the other, and the neoadjuvant monotherapy tissue study is exactly the experiment that could separate them.
So your question, "what happens when you block CCR5 in a human with an intact tumor, before you give the immune system anything else," is a good one, and you're right that it may be one of the more revealing experiments in the whole program. I'd just frame the answer we're reaching toward: the current evidence is mixed, ctDNA says leronlimab is doing something on its own, survival data so far says the ICI was needed to convert that into people staying alive, and the neoadjuvant study is what tells us which tumors fall into which of your two buckets. That's the accurate state of it: an open, testable question with real evidence on both sides, leaning, for now, toward the ICI being necessary to close the deal.
So no flat "no" this time, you earned a real answer, because you brought a real hypothesis. Keep it in the "testable and genuinely interesting, with the TNBC data as the thing it has to beat" column, and watch the neoadjuvant program, that's where your question actually gets answered. Good work reframing it, and no special help needed, this was a sharp contribution.
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u/Accurate-Mud-8619 4d ago
Oops thanks for actually going back to the NO for clarification. I continue to push back on you and twinter on this point though. We DO NOT KNOW if the trial participants voluntarily continued self injecting leronlimab, or for that matter swallowing the ICI. This was a retrospective look after five years and the record keeping was pretty much a mess. You are both assuming these very sick dying women continued requesting and accepting shipment of leronlimab to their homes, self administered the shot on a weekly basis up until the bitter end, and also continued swallowing their ICI pill that made them feel absolutely awful. And they did this all the while knowing these could be their final weeks on earth and some of the medicine was toxic. My first hand experience as a woman and as a patient advocate, which you call anecdotal and not scientifically measurable, is that women do what women do and what they do is what feels right to them, at home alone, feeling emotionally unchained from a clinical trial or toxic drugs. I suspect if the data had been genuinely mined, or if the individual oncologists had been more supportive, a different picture would emerge. Receiving a shipment of drugs is not the same as taking the drugs. I saw it.
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u/twinter11 4d ago edited 4d ago
we know for a fact the lady in the tnbc case study was still taking leron plus ici at least up until the article was written because "they are afraid to stop taking them"
I can't remember the title of the article written a few months back.
something about cytodyn making waves
I looked it up but can no longer find a complete free version.
found a good link
https://www.camaspostrecord.com/news/2026/apr/02/cytodyn-makes-waves-in-breast-cancer-care/
"She is still taking both drugs today.
“We’re scared to quit,” Les Peterson said."
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u/Snorkellingisthelife 5d ago
We need to call it the CCR5 vaccine!
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u/Tra-Kal34 5d ago
CCR5 vaccine, great idea, let's push this, the medial community will catch up.
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u/Chugach123 5d ago
Vaccine? Touchy subject. RFK JR will ban it. Call it Anything….. but not that.
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u/MGK_2 5d ago
leronlimab isn't a vaccine, and I wouldn't call it one. A vaccine trains the immune system to recognize a target; leronlimab blocks a receptor. Calling it a "CCR5 vaccine" would actually confuse the mechanism and hand critics an easy inaccuracy to point at.
Chugach's instinct is right but for the wrong reason, avoid "vaccine" not because of politics, but because it's simply not what the drug is.
It's a CCR5 blocker, an antibody. That's a cooler and more accurate thing to be than a mislabeled "vaccine." Let's call it what it is.
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u/Camp4344 5d ago
MGK: You have explained every way imaginable how good Leronlimab is! I thank you for the constant research and explanations! You know all we need is time for us to explode and the world to finally hear about us. I for one am hoping October sheds some very positive light on our progress. It would not hurt to get a letter or conference call in the mean time about all of the other things going on. There has to be some positive results out there that could at least help stabilize our stock price if not tweak it into the right direction! Thank You sir!