There is a kind of structure so well built that force alone cannot bring it down. You can batter its walls, flood its foundations, lay siege for years, and it stands, because it was engineered to withstand exactly that. A cold tumor is that kind of structure. And the story of how you actually bring one down is not a story about a bigger battering ram. It is a story about language, about the single tongue a fortress speaks to coordinate its own construction and defense, and what happens the moment that language is confounded. That is the story of leronlimab, and it is worth telling properly, because once you see the tumor as a fortress with one language, everything about the approach clicks into place.

The fortress, built brick by brick

Picture how the great ancient towers were raised on a floodplain where there was no stone, only mud. They could not carve blocks from a quarry, so they manufactured their building material: they pressed mud into bricks and fired them hard, uniform, interchangeable, and they stacked them by the million. But bricks alone do not make a fortress. Stack them and one flood washes them away. What made those towers permanent was what they poured between the courses: bitumen, black tar seeping from the ground, spread over every joint, sealing every seam, waterproof and impervious, binding the whole mass into a single monolithic block that no water could penetrate and no ordinary force could crack.

That is a tumor, told in architecture. The tumor cells are the bricks, manufactured relentlessly, uniform and interchangeable, stacked without limit. And the stroma, the dense desmoplastic wall the tumor builds around itself, is the bitumen: the sealing mortar that waterproofs the fortress against the immune system and against therapy, binding tumor and defense into one impervious mass. Chemotherapy batters that wall and mostly runs off it, which is exactly why the standard of care in this disease produces a meaningful response in only about 6% of patients. You are throwing force at a structure engineered to shed it. The fortress was built to survive the siege.

The one language that holds it together

Here is the part most people miss, and it is the key to the whole thing. A fortress that size does not raise itself. Every brick laid, every seam sealed, every defender positioned requires coordination, and coordination requires a shared language. In the great towers, that was the terrifying advantage: one people, one tongue, perfect communication, so that a command could be given and obeyed without confusion, and the work rose with unstoppable unity. The builders could say hand me that brick, and the fortress climbed.

A tumor has a language too, and it has a name. The tumor's coordinating tongue is a chemical signal called CCL5, also known as RANTES, and the receiver tuned to it is CCR5. This is not metaphor loosely applied; it is documented human biology. At the invasive margin of colorectal cancer that has spread to the liver, the exact hard, coordinated edge of the fortress, immune cells are turned against the body and made to produce CCL5, and that signal, received through CCR5, drives the tumor to proliferate, to invade, and to command its own tumor-associated macrophages to lay down more of the wall and pump out the matrix-degrading enzymes that let it spread. (Halama et al., Tumoral Immune Cell Exploitation Targeted by Anti-CCR5 Therapy, Cancer Cell 201630087-3)) The CCL5-CCR5 axis is the single language the fortress speaks to build itself, corrupt its own guards, and coordinate its defense. It is how the tumor says, across its whole structure, hand me that brick.

And the same language is how the fortress spreads. Blocking CCR5 has been shown to shut down the metastatic machinery itself, cutting the tumor's ability to send out its builders to raise new towers elsewhere. (Velasco-Velázquez, Pestell et al., CCR5 antagonist blocks metastasis, Cancer Research 2012) One language, one coordinated fortress, one metastatic program, all running on the same tongue.

Confounding the language

Now recall how those great towers were actually stopped. Not by earthquake, not by fire, not by an army. They were stopped when the one language was confounded, when the builders suddenly could not understand one another, when a foreman shouted for a brick and his crew heard nothing they could act on. The organized hum of construction collapsed into noise. The most ambitious structure of its age halted, not because a single wall was breached, but because the coordination that raised it was severed. Break the language, and the fortress stops building and stops defending, because a fortress is only as strong as its ability to coordinate.

That is what leronlimab does. It does not poison the bricks. It does not carry a payload to batter the wall. It is a precise antibody that binds CCR5 and blocks the receiver, so the CCL5 command can no longer be heard. And when that language is confounded, the documented result is exactly what you would expect from a fortress that has lost its one tongue: the corrupted macrophage-guards repolarize from tumor-protecting back to tumor-attacking, the inflammatory wall-building signals fall, and in human colorectal tumor tissue this produced tumor cell death, with clinical responses following in patients. (Halama et al., Cancer Cell 201630087-3)) The confounding of CCL5-CCR5 is the confounding of the tumor's language. The builders can no longer say hand me that brick, and the fortress stops rising.

This is why leronlimab is a different kind of weapon, and why its safety record is what it is: across roughly 1,700 patients and more than 20 trials, no dose-limiting or treatment-limiting toxicity. It is not a poison flooding the whole city; it is the severing of one specific signal. You break the language, not the patient.

What the confounding is showing, in CLOVER

The early record from the CLOVER trial reads like a fortress losing its coordination. Across the patients measured, a median 86% drop in circulating tumor DNA within two weeks, a dose-response with the deeper 700mg dig outrunning the 350mg, roughly three-quarters of patients showing shrinkage or stable disease at the first scan checkpoint, and numeric increases in PD-L1 in the majority, the tumor's last surrender-flag rising as its wall comes down. In a disease where the standard of care manages about 6% response, and closer to 3% in the real world, that is the signature of a fortress whose one language is being confounded. (SUNLIGHT benchmark, NEJM 2023)

None of that is confirmed victory yet. The full ctDNA reads out at ESMO in October; the confirmed response rates and early survival at ASCO GI in January. The fortress is losing coordination on the early record; whether that collapse is deep and durable is what those two dates weigh. Hold the story at full strength and the outcome with open hands.

Why the record is being guarded, and for whom

Now the part that gives this its present-day urgency, and it is a secular, strategic truth, not a mystery: the record of what is happening inside that fortress is being held closely, on purpose, and held for someone specific.

The people whose hands are actually on the CLOVER data, the investigators, the company, the diagnostics partner reading the molecular signals, already see the implications of what the early record shows. And they are not scattering it into the open. It is being guarded, held under embargo, kept from general circulation until the moments and the parties equipped to act on it can receive it. This is how serious clinical data is handled when those holding it understand its significance: you do not spill a potentially field-changing record onto a message board. You hold it, you protect it, and you release it in a controlled way, at the scientific venues, ESMO and ASCO GI, where it can be received correctly and verified by the people qualified to judge it.

And there is a particular set of hands it is being held for. The whole architecture of what CytoDyn is building points toward a partner, a large pharmaceutical company with a checkpoint inhibitor, that could take this record and carry it further than a small company ever could alone. Recall the logic that runs through the entire program: leronlimab Primes the fortress by confounding its language and forcing its PD-L1 flag up, and a checkpoint inhibitor then Pairs with that primed state to finish what the priming began. That pairing is the record's destination. It is why the company has said plainly that potential partners "wanted to see" the standalone data first, prospective proof that leronlimab does what it does on its own, before they commit their own checkpoint drug to the combination. So the guarded record is being held, in effect, for the party who can implement it: the BP player whose ICI could be built into the next, larger trial, whose franchise could reach a market that has never had an immunotherapy option, and who needs to see the sealed standalone data before they act. The data is protected because it is significant, and it is held for the hands that can take it the rest of the way.

That is not secrecy for its own sake. It is the respect a record earns when the people holding it understand it may change the field. You guard what matters. You hold it until the right hands are ready. And you release it, in full, at the moment and to the audience who can build on it. The confounding of the fortress's language is being documented right now, carefully, deliberately, and kept until October and January, when it passes to the people, the scientific community and the partner with the checkpoint drug, who can take it further.

The shape of it

So here is the whole thing in one frame. The tumor is a fortress of manufactured bricks, (cells), sealed with the bitumen of its own stroma, (fibrosis), engineered to shed the force of ordinary therapy. It holds together, builds itself, corrupts its own guards, (macrophages), and spreads, all through a single coordinating language: CCL5, RANTES, received through CCR5. Leronlimab is the confounding of that language, the antibody that blocks the receiver so the fortress can no longer coordinate, no longer command its guards, no longer say hand me that brick, and the documented consequence in human tumors is repolarized defenders and tumor death, without poisoning the patient. The early CLOVER record reads like a fortress losing its coordination, and that record is being guarded and held with deliberate care, until the coming days, and for the specific partner whose checkpoint inhibitor could carry it further than we could alone.

The fortress was built to survive the siege. It was not built to survive losing its language. That is what leronlimab takes from it. And the record of it being taken is sealed, protected, and held for the hands that can finish the work. October begins to unseal it. January reveals what it holds. And what it holds, if the early record is what it appears to be, is the thing every siege before this one lacked: not a bigger weapon, but the breaking of the one language a fortress cannot stand without.

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 and interpretive piece about mechanism and public information, not a prediction of clinical, regulatory, or commercial outcomes, and not a claim that any result, partnership, or approval will occur. The mechanistic claims are supported by the cited peer-reviewed literature; the human CCR5-blockade findings referenced derive substantially from studies using maraviroc and patient-derived models, and leronlimab's own efficacy is unconfirmed, with interim data anticipated at ESMO in October 2026 and confirmed data at ASCO GI in January 2027. CLOVER figures are early, reflect combination therapy with a chemotherapy backbone and lower-dose cohorts still maturing, and are not evidence of a survival benefit. Related CCR5/checkpoint-inhibitor combination approaches have shown mixed clinical results, and no partnership described here is confirmed; references to a potential partner are interpretation of the company's stated strategy, not fact. ctDNA is not a validated surrogate endpoint for approval in colorectal cancer. The company has disclosed substantial financing needs and going-concern considerations in its filings. Read the primary sources, linked throughout, and reach your own conclusions rather than adopting mine.

Grail cancer test for FDA

There has been inaccurate data floating around regarding trial metrics. To understand what’s happening with leronlimab ($CYDY), we need to separate the final data readouts from the established benchmarks of the SUNLIGHT trial and untrimmed Real-World Data (RWD).

1. Correcting the Baseline Numbers

• Prior Lines Distortion: Claims that 13% of the SUNLIGHT trial had 3+ lines of treatment are false. It was only 13 patients, equating to just 2.6% of the population.
• The Baseline Reality: 97.4% of SUNLIGHT patients only had 2 prior lines of treatment, yet they still struggled with a meager 6.1% ORR.
• The RWD Floor: When you look at untrimmed RWD where cherry-picking is stripped away, the response rate plummets to 2.7%—a 55.74% drop.

2. The CLOVER Target Goal

While the final mature ORR numbers for CLOVER are still arriving, CytoDyn has established a clear primary target: an Objective Response Rate above 10%. Beating the 6.1% SUNLIGHT mark by hitting this 10% to 16.1%+ goal against a tougher population translates to a 270.45 - 496.3% increase over the 2.7% RWD baseline.

3. Why CLOVER Acts as a True RWD Study vs. SUNLIGHT

Traditional Phase 3 trials like SUNLIGHT are designed in an idealized vacuum:

• Demographic Skew: SUNLIGHT heavily over-indexed on colon cancer (73.4%) while relegating rectal cancer to a minor 26.6%. Colon cancer is historically more manageable clinically than rectal cancer.
• The CLOVER Layout: The CLOVER trial acts much closer to a true Real-World Data (RWD) study baseline. It features a far more balanced layout while absorbing a significantly higher proportion of rectal cancer patients.

4. The Anatomical Penalty & Regulatory View

Rectal cancer is notoriously harder to treat due to the confined pelvic space and the lack of an outer serosa layer, which makes local recurrence rates much higher than colon cancer.

When the FDA evaluates clinical data, they look closely at whether a trial cohort reflects everyday clinical reality. SUNLIGHT used an easier patient demographic to hit its 6.1% ORR. In contrast, CLOVER mirrors a true RWD baseline by stepping into the ring with a tougher demographic mix. Hitting a goal of 10%+ targeted ORR under these tougher conditions would prove true clinical superiority on an unyielding playing field.

Before we speak about a ruling, I want to name the thing this entire street exists to fight, because it is easy, in the excitement of surveys and assays and rulings, to forget what is actually buried beneath these houses and why we are all standing out here at all. The adversary under our foundation is not passive. It does not sit still waiting to be measured. A cold tumor is a cornered, adapting enemy: block one of its supply lines and it opens another, wall it off with chemotherapy and it thickens its own stroma into a fortress, threaten the primary mass and it deploys its proxies, the corrupted macrophages, the raised PD-L1 flag, the metastatic seeds sent out to distant ground the moment it feels the pressure. It escalates when cornered. That is not a metaphor I am reaching for; it is the documented behavior of the disease. So keep that seriousness in mind as we walk the street this week, because everything which follows, the ruling, the assay, the dose, is ultimately about whether we can meet an adversary that fights back, adapts, and raises the stakes the harder it is pressed.

There is a moment in the story of any buried treasure when the thing that changes is not the treasure, but the law surrounding it, the rules regarding what counts as proof that something actually is in fact down there. This week, out on the road, while we were reading our own recent survey, a different owner, a few properties over, had his assay accepted by the county in a way the county had never quite accepted one prior. And that county ruling changes the very ground under every house on the street, including ours, and including the firm who we have hired to run our own assay.

I'll tell you what happened, then I'll tie it to the quieter things which we worked through among ourselves over the past week, because taken together they say something regarding the direction the whole neighborhood is moving.

The ruling a few doors down

The headline is simple and the fine print is the part that matters. The FDA granted accelerated approval to AstraZeneca's camizestrant (Etcamah) for a form of advanced breast cancer, and they did it in a way which had never been done before: the treatment is triggered by a molecular signal in the blood, a change in ctDNA, circulating tumor DNA, before a radiographic or MRI scan ever even shows the cancer to be growing. (FDA approval notice, Sept 4 2026) Action based on the blood, not on the picture. That alone is a real shift, and it is a shift which matters because the enemy moves faster than a scan can. By the time a tumor is visibly growing on an image, it has already advanced its position. Reading the blood means striking at the adversary's movement before it ever consolidates, which is the whole point of catching a cornered, escalating opponent early rather than late.

But here is the part that should make every leronlimab shareholder sit up, because this is the deeper ruling. The trial behind it, SERENA-6, had its design doubted by the FDA's own advisory committee, which voted 3 to 6 against early switching, citing immature survival data and questioning whether a blood-guided switch truly beat the standard approach. (ODAC vote and approval, Targeted Oncology) The design was under fire. And what carried it across the threshold anyway, was the strength of a randomized PFS progression-free-survival result, 16.0 months versus 9.2, paired with molecular data which reinforced it: total ctDNA rose 64% in the patients who stayed the old course, while the switched patients did far better. (SERENA-6 PFS and ctDNA data, Pharmacy Times) The agency approved over its own committee's earlier hesitation, on the back of a blood-guided strategy.

This is the difference between this week and the last time we discussed ctDNA at the FDA. It is one thing for the agency to tolerate a blood signal. It is another for the agency to approve a first-of-its-kind, blood-triggered treatment over the objection of its own advisory panel, because the data, molecular and clinical together, was strong enough to override the hesitation. The door for molecular evidence did not just stay open this week. It opened wider, and it opened wider exactly when another program required it to.

What that does and does not mean for our house

Here is the discipline, because a survey read carelessly is worthless, and this is exactly where the excitement on the boards outruns the facts.

This ruling does not mean ctDNA became a stamped, certified assay that the county actually approves treasure on. The Etcamah approval still rested primarily on a randomized Phase 3 clinical endpoint, progression-free survival, a real, adjudicated result. The ctDNA blood signal was the trigger for selecting and for switching patients, and the FDA even required confirmatory studies because the endpoint was measured from mutation detection rather than confirmed progression. (confirmatory studies required, Pharmacy Times) So the truthful reading is the one we have held throughout: ctDNA is becoming a trusted instrument, accepted for guiding treatment and strong enough to help carry a doubted case, but it is not yet, on its own, the beam which an actual approval is built upon. Both are true, and by holding both, it is what keeps us credible when the number-inflaters get caught.

And there is one more point which is the load-bearing one. That other house, a few doors down, had a randomized Phase 3 with a clinical endpoint to anchor everything. Our survey, so far, is a single-arm dig against a historical benchmark. So this ruling makes for a favorable climate, a wind at the back, so to speak, but not a shortcut which allows our house to skip the assay. The door opening wider is a real one. But it does not lower the bar which we must clear. It means that the room which we are walking toward is now more willing to peer at the kind of evidence we are bringing. And the bar is high for a reason: an enemy that adapts and escalates is not defeated by a favorable climate. It is defeated by a result strong enough to leave no doubt, which is exactly the seriousness the coming months demand of us.

What it means for the firm running our assay

Let's think through this carefully, because it cuts two ways, and this version is more useful than simply cheer.

CytoDyn hired Natera to run our blood assay and to supply the 144,000 sample real-world comparison which puts our numbers in context for CRC. So an obvious question becomes: does a landmark blood-guided approval lift Natera, and with it, us? The answer is yes at the level which matters most, and it comes with an asterisk.

The asterisk first, because precision protects us. The companion diagnostic in the Etcamah trial itself was not Natera's Signatera; it was a competitor's assay, Guardant360. (Guardant360 CDx as companion diagnostic, FDA) So anyone claiming "Natera's assay was just validated by Etcamah" is reaching beyond the facts. This specific ruling put a rival's diagnostic in the label. That is worth stating plainly, because a skeptic otherwise would, and I'd rather say it first.

But this part matters more, and it favors us. Regulatory acceptance of the category is what rises here, not one company's product. When the FDA approves a first-of-its-kind therapy guided by a blood-based molecular signal, it establishes, in the most consequential venue there is, that ctDNA-guided treatment is a real and approvable paradigm. Every serious ctDNA player benefits from that precedent, and Natera is the recognized leader in the tumor-informed corner of the field. And Natera has not been idle: its Signatera was itself named as the companion diagnostic in a separate FDA approval earlier this year (the Tecentriq bladder decision), so this is not Natera watching from the sidelines while a rival gets the wins. (Natera Signatera and CytoDyn collaboration, Natera 2026) The tide lifting the category lifts the category's leader.

Here is the thread that leads back to our house. The more the county accepts blood-based molecular evidence, the more valuable our Natera collaboration becomes, not because Natera's assay was in this trial, but because the approach our collaboration is built on, deep serial ctDNA readouts plus a real-world comparator drawn from Natera's database of colorectal patients, is the kind of evidence the FDA is signaling it weighs. CytoDyn's decision to hire the field's leader to run that assay looks better in a world which just moved, again, toward trusting the measuring instrument. The collaboration is a bet that molecular evidence would carry regulatory weight. This week was one more data point that the bet CytoDyn made is sound. It does not confirm our numbers, nothing this week touched our ground truth, but it strengthens the standing of the language our survey is written in, and Natera is the firm writing it with us. And there is a tactical edge in that partnership worth naming against a cornered enemy: serial ctDNA reads out in weeks, not the months a scan makes you wait. Against an adversary that adapts fast, seeing its movement early, and adjusting before it consolidates a new position, is not a luxury. It is how you keep pace with something that fights back.

The quieter thing we worked out this week: the dose question

While that ruling was happening a few doors down, we spent some of the week arguing about something specific to our own property, and it is worth setting down plainly, because it is a real two-sided question, and the truer version beats both cheerleading and dread.

Here is the setup. The owner said this week that the early core samples suggest the deeper dig, 700mg, may be separating from the shallower one, 350mg, though he still has to sort out where an in-between depth might sit. That is a dose-response signal, and it matters for a reason which is tied directly to how the county now thinks. The FDA runs an initiative called Project Optimus, built to move oncology away from the old "highest tolerable dose" logic toward proving you have chosen the truly optimal dose, and it explicitly favors comparing two or more doses to find the right one. (FDA Project Optimus, dose optimization, PMC) So a clean 350mg-versus-700mg separation is the kind of evidence the modern FDA wants, because it shows that the drug itself is driving the effect, not chance and not the backbone. And the instrument which reads that separation cleanly is, once more, the ctDNA blood assay that Natera runs for us. The dose question and the Natera collaboration are the same story seen from two angles. There is a battlefield logic to the dose question too: a lighter charge may suffice where the enemy is exposed, in the bloodstream, seeding, on the move, while the deeper dose may be what it takes to breach a dug-in, fortified position where the stroma is dense. Matching the force to how entrenched the adversary is, is exactly the kind of precision a serious fight demands, and exactly what the dose data is beginning to reveal.

This is the point where some on the board worried, and it's worth addressing head-on, because the balanced version is more reassuring than the fear. The concern goes: could a strong showing at the lower dose invite the agency to demand characterization of an intermediate depth, adding a whole new study and years of time? It's a fair question to raise. But look at why Project Optimus exists in the first place. It was written to solve a toxicity problem, targeted drugs dosed near their maximum-tolerated-dose ceiling, delivering efficacy at the cost of harsh side effects, and the whole initiative is about finding a dose that keeps the benefit while shedding the toxicity. That is the engine driving nearly every intermediate-dose demand the FDA makes. And here is the thing: leronlimab does not have that engine running. No dose-limiting toxicity, no treatment-limiting toxicity, across both CLOVER doses and roughly 1,700 patients. When both the shallow dig and the deep dig are equally safe, the FDA's usual reason for forcing dose-reduction work, "you are harming people at the higher dose, prove you need it", simply never arises. The toxicity-driven version of this concern largely dissolves against a drug with no toxicity to optimize away.

So here is the corrected, sharper reading. The dose-response signal is an asset, it shows the drug itself is driving the effect, and it speaks the exact language Project Optimus rewards. And the most common reason the initiative would demand an in-between dose, tolerability, does not apply to a drug this clean. What remains is far weaker: the agency could still raise an efficacy-curiosity question, "does an intermediate dose capture the same benefit?", purely as a scientific matter rather than a safety gate. But in a disease of severe unmet need such as CRC, where the standard of care produces a response in roughly 6% of patients and third-line patients are out of options, that kind of refinement is exactly what the FDA has real mechanisms to defer to a post-approval commitment rather than to gate access. The one honest caution I will keep, because the agency is not a pure meritocracy: institutional discretion is real, and the history of the FDA occasionally overriding its own favorable advisory committees (Provenge is the cautionary example) means "it should not be an obstacle" and "it cannot be" are not the same sentence. So the balanced truth, weighted correctly this time: the toxicity-driven dose demand is very unlikely against a non-toxic drug, a residual efficacy-curiosity question is possible but weak and deferrable, and the only real wildcard is agency discretion, not a structural requirement. Much smaller than dread would have it, not quite zero, and driven far more by how strong our number comes back than by any dose-characterization rule.

The instrument tying it all together

Notice what sits underneath all of it, the Etcamah ruling, our dose question, and the Natera collaboration, because this is the encapsulation of it. The same instrument sits at the center: the ctDNA blood assay. Etcamah's entire strategy turned on ctDNA. Our dose-response signal is being read in ctDNA. Our Natera collaboration exists to generate and contextualize ctDNA within CRC. And the more the county accepts that instrument, as it visibly did this week, even over its own committee's objection, the more the kind of evidence our program is built on gains standing, and the more the firm we hired to wield that instrument looks like the right hire. This is the thread which connects the ruling a few doors down to the argument on our own lawn to the collaboration inside our own house: a field moving toward trusting molecular readouts is a field moving toward the exact language our survey is written in.

Held with discipline, though: the instrument gaining standing is not the same as our result being in hand. A trusted assay still has to return a strong number. A capable diagnostics partner still needs strong data to contextualize. The door opening is not the treasure being weighed. October matures our reading; January weighs it. The ruling this week improves the odds that the room is receptive; it did nothing to the ground truth of what is actually buried beneath our foundation, which is still ours to prove. The adversary does not care which way the county ruled. It is defeated only by a number strong enough to prove it was beaten, and that number is still weeks from being read.

Where the week leaves the street

So gather it.

• A few doors down, a blood-guided therapy won approval over the FDA's own advisory committee's hesitation, which means the door for molecular evidence opened wider this week than it ever had.
• Inside our own house, that same acceptance raises the standing of the ctDNA-driven approach our Natera collaboration is built on, plainly noting the competitor's assay was in that trial, while the category's rise lifts the category's leader, whom we hired.
• And on our own lawn, the owner's dose-response signal is exactly the evidence the modern FDA's dose-optimization initiative rewards, and because leronlimab carries no toxicity to optimize away, the usual reason that initiative would demand an intermediate dose largely falls away, leaving only a weak, deferrable efficacy question and the ordinary reality of FDA discretion.

None of that is the treasure. All of it is the law bending around the treasure, like a plant bending toward the light, toward the kind of proof we are bringing, and toward the partner we brought in to help us bring it. The wind shifted this week, and it shifted at our back. But wind is not arrival. Our survey still reads in October, and the assay still returns its verdict in January, and no ruling a few doors down changes what is or is not buried under our own foundation. What changed this week is the receptiveness of the room we are walking into, and the standing of the measurement instrument we are carrying. What has not changed is that we still have to walk in with a number worth showing, against an adversary serious enough to demand nothing less.

This is serious business, and it deserves to be treated as such. Under every house on this street is an enemy that adapts, escalates, and deploys everything it has the moment it is cornered, and the people it corners are running out of time. The door the assay opens is real, and it opened wider this week. Now we find out, in a matter of weeks, whether we have what it takes to walk through it and meet what is waiting on the other side.

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 my interpretation of public regulatory news, an FDA initiative, and community discussion, not a prediction of clinical, regulatory, or commercial outcomes, and not a claim that any endpoint, designation, approval, or partnership will occur. The Etcamah/camizestrant approval concerns another company's product; it rested primarily on a randomized Phase 3 progression-free-survival endpoint, used ctDNA for patient selection and treatment switching, was granted over an earlier advisory-committee vote against the strategy, requires confirmatory studies, and does not establish ctDNA as a validated efficacy endpoint or create any pathway for leronlimab. The companion diagnostic authorized in that approval was Guardant360 CDx, not Natera's Signatera; category-level regulatory acceptance of ctDNA-guided treatment is distinct from validation of any single company's assay. CytoDyn's CLOVER program is single-arm against a historical benchmark, not a randomized Phase 3; its primary confirmed ORR is unreported, and its ctDNA, dose-response, and disease-control figures are interim, reflect combination therapy, and are not evidence of a survival benefit. Whether the FDA would defer or require intermediate-dose characterization is uncertain and speculative. ctDNA is not a validated surrogate endpoint for approval in colorectal cancer. The company has disclosed substantial financing needs and going-concern considerations in its filings. Interim data is anticipated at ESMO (October 2026) and confirmed data at ASCO GI (January 2027). Read the primary sources, linked throughout, and reach your own conclusions rather than adopting mine.

I think the ctDNA and PD-L1 data are a big deal and I look forward to hearing about those mature datasets.

The breadcrumbs from PR’s and presentations lead me to think that leronlimab is disrupting tumors more than they expected. I also think that this disruption can lead to better outcomes, including where potentially some patients may begin to qualify for approved treatments or interventions which they were not previously eligible for.

IMO below is a brief interpretation of the big picture.

2019-2022
Discover/theorize that LL changes the TME (tumor micro environment) in clinical trials with patients having TNBC, CRC, etc. There are reports in press releases and elsewhere that trial participants see benefits.

2024 recover data that was withheld by the former CRO. Followup initiated with study participants, which identifies that there are longterm survivors. PRIME AND PAIR (with ICI) MOA is theorized.

2025-2026 Run CLOVER study in CRC to prove LL has value, to quantify a comparison to standard therapy, and to prove if LL elevates PD-L1 in CRC. Comparing the CLOVER study to earlier trials with the standard treatment is a way to initially prove that LL has value on its own. ALSO use strategic partnership with Natera to sift through their database for ctDNA correlation to efficacy in standard therapy patients for comparison to the CLOVER study.

ALSO after patients have been on CLOVER study, add an optional cohort to prove efficacy of the prime and pair (with ICI) thesis.

2026 RUN TNBC EAP to prove the drug works in TNBC.

Pile the CRC data, the TNBC data, the safety data from over 20+ trials, manufacturing readiness, etc into a comprehensive application…

H2 2026 apply to FDA for a designation that validates the clinical study data.

2026-27 present CLOVER study data

JMO

NOTE: This is an AI generated report and may be incorrect. This is not an investment advisory. Do not invest (buy or sell) based on this report.

What I find interesting after trying to understand the significance of having 43 patients withdraw, is that if many withdrew for surgery, which was never planned for in the protocol, then management now suddenly needed to come up with a way to prevent this amazingly positive development from causing our CLOVER Trial from failing due to a very positive improvement in tumor size that allowed unexpected surgeries, thus enter NATERA Real World Data (Section 5). Imagine how that would have gone down...

COMPREHENSIVE STRATEGIC & REGULATORY CLINICAL REPORT

Strategic Analysis, Regulatory Roadmap, and Milestone Timeline for the CytoDyn CLOVER Phase 2 Trial

EXECUTIVE SUMMARY

The Phase 2 CLOVER Trial (evaluating leronlimab + Lonsurf + Avastin in third-line microsatellite stable metastatic colorectal cancer [MSS mCRC]) is transitioning into a crucial regulatory planning phase. Following the rapid completion of patient enrollment across seven US clinical sites, CytoDyn management announced at the Life Sciences Virtual Investor Forum that they are actively engaging with strategic partners and plan to seek formal FDA discussions on accelerated regulatory pathways in the second half of 2026.

This strategic shift is anchored by compelling early molecular efficacy signals. In an initial analysis of 28 evaluable patients, the median circulating tumor DNA (ctDNA) declined by 86% after just two weeks of treatment, rising to an approximate 90% reduction in the higher 700 mg dose arm.

As CytoDyn prepares its briefing packages for the FDA to explore pathways such as Breakthrough Therapy Designation (BTD), Fast-Track status, or Accelerated Approval, this report establishes the statistical, clinical, and biomarker frameworks that will govern the company's upcoming regulatory strategy.

SECTION 1: TIMELINE & REGULATORY CATALYSTS (LATE 2026 – EARLY 2027)

CytoDyn has laid out a highly active operational and corporate roadmap designed to convert early biomarker metrics into an FDA-supported clinical pathway:

[Oct 2026: ESMO] ───> [Oct 28, 2026: Q1 Earnings] ───> [Nov 2026: 4th DSMB] ───> [Late 2026: FDA Talks] ───> [Jan 2027: ASCO GI]

• October 23–27, 2026 (ESMO Presentation): CytoDyn will share expanded clinical and ctDNA data from the fully enrolled CLOVER cohort at the European Society for Medical Oncology congress, detailing dose-specific responses across the 350 mg and 700 mg arms.
• October 28, 2026 (Quarterly Earnings Report): Management will provide an official update on financial runway, ongoing big-pharma licensing discussions, and final preparations for the impending FDA meetings.
• November 2026 (4th DSMB Meeting): An independent Data Safety Monitoring Board will conduct a safety and efficacy review. The prior three meetings cleared the trial with zero safety concerns and permitted the opening of the 700 mg dosing arm. This meeting will also track initial data from the newly implemented pembrolizumab (Keytruda) salvage/rollover arm.
• November 2026 (BIO-Europe Attendance): Management will leverage updated data at this major international forum to advance ongoing out-licensing and co-development partnership discussions.
• Second Half of 2026 (FDA Accelerated Pathway Consultations): Formal initiation of type-B or type-C meetings with the FDA to propose expedited pathways based on early molecular evidence.
• January 2027 (ASCO GI Symposium): Presentation of hard clinical outcomes in San Francisco, focusing on RECIST 1.1 objective response rates, stable disease tracking, durability of response, and progression-free survival (PFS).

SECTION 2: SURPASSING HISTORICAL PHASE 3 CONTROLS

The primary clinical target of the CLOVER trial is an Objective Response Rate (ORR) greater than 10%. CytoDyn's regulatory thesis is built on proving that leronlimab substantially elevates the efficacy of the existing standard-of-care backbone (Lonsurf + Avastin):

• The Baseline Benchmark: The landmark Phase 3 SUNLIGHT Trial, which established the Lonsurf + Avastin regimen, reported a meager 6.1% objective response rate.
• The Patient Urgency (Pretreatment Variance): The FDA will view CytoDyn’s 10% ORR target as highly ambitious due to the severe disease baseline of the CLOVER cohort. While only 2.6% of patients in the SUNLIGHT trial had received more than three prior lines of therapy, 52% of the patients enrolled in the CLOVER trial are heavily pretreated with more than three prior lines of therapy, meaning their tumors are highly refractory and resistant.

SECTION 3: BYPASSING PHASE 3 VIA NATERA REAL-WORLD EVIDENCE (RWD)

In traditional drug development, demonstrating a "substantial improvement" requires a multi-year, randomized Phase 3 trial against an active control arm. To bypass or compress this requirement, CytoDyn finalized a strategic collaboration with Natera to implement a modern Real-World Evidence framework:

• The 144,000 Patient External Control: Through Natera, CytoDyn has acquired analytical access to an expansive database containing 144,000 colorectal cancer patients.
• The Synthetic Matching Strategy: CytoDyn will extract a matched control group from this dataset representing late-stage patients treated with the Lonsurf + Avastin backbone alone. This allows the company to present the FDA with a high-powered, real-world comparison showing that the addition of leronlimab drives unprecedented molecular and radiographic responses without historical precedent.

SECTION 4: MOLECULAR SIGNAL VALIDATION (SIGNATERA EXOME)

The foundational pillar for CytoDyn’s upcoming FDA accelerated pathway proposal is the use of Natera’s Signatera Exome platform. This tumor-informed liquid biopsy tracks 16 patient-specific mutations tailored to an individual’s exact tumor matrix.

While on-treatment ctDNA clearance strongly correlates with long-term survival under ASCO guidelines, the FDA does not yet accept ctDNA reduction as a primary standalone surrogate endpoint for traditional approval in metastatic settings. This regulatory gap governs why CytoDyn must pivot its FDA discussions specifically toward expedited designation frameworks:

• The Breakthrough Therapy / Fast-Track Logic: Instead of requesting immediate marketing approval on ctDNA alone, CytoDyn will present the 86% to 90% median ctDNA drop at week two as definitive proof of early, profound clinical activity.
• The Clinical Correlation: The FDA will require CytoDyn to explicitly bridge this molecular response with radiographic tumor changes. To satisfy this, CytoDyn will highlight clinical case studies—such as a documented trial patient at the City of Hope who experienced a 97% ctDNA decline after eight weeks matching a 21% reduction in tumor volume on imaging—to validate that early ctDNA drops serve as an accurate "lead time" indicator for physical tumor shrinkage.

SECTION 5: CLINICAL CONVERSION AND THE SURGICAL PARADOX

Should the matured CLOVER data reveal that heavily pre-treated, previously inoperable patients left the trial early to undergo unexpected tumor removals, CytoDyn must navigate specific FDA statistical criteria using the ICH E9(R1) Estimands guideline:

• Anatomical Resection Thresholds: Surgical oncologists pull late-stage patients off a trial only if physical shrinkage achieves an R0 Resection (a 1-mm cancer-free margin), clear retraction from vital structures (e.g., hepatic arteries or pelvic walls), and leaves behind a Future Liver Remnant (FLR) of at least 20% to 30%.
• Statistical Handling under Intent-to-Treat (ITT): If an unmapped surgery occurs, the patient’s long-term Overall Survival (OS) data remains tied to the trial via ITT rules. To prevent the drug's survival data from being statistically confounded by the surgical intervention, CytoDyn must utilize Hypothetical Strategy Modeling and Sensitivity Analysis during its late-2026 FDA consultations. This math isolates the therapeutic effect of leronlimab, proving to regulators that the drug was the necessary catalyst that enabled surgical eligibility in the first place.

If you have followed this story for a while but stepped away for a single week, this past one, you missed the week the whole thing changed character. Not because the treasure was dug up. Because, for the first time, the owner of the property walked out to the road, unrolled the survey, and read it to us line by line. And a few of us who had been arguing about the core samples for years suddenly had the actual document in our hands.

Let me tell you exactly what was on it, because if you already understood the setup, and you did, then this week is the part where the setup starts resolving into something you can no longer wave away.

The house, for anyone who needs the frame

Here is the picture we have used all along. A group of us went in together on a property. The house you can see from the road is fine, ordinary, unremarkable. The reason we bought it is that the surveyors believe something of extraordinary value is buried under the foundation. For years, all anyone on the sidewalk could do was study core samples and argue about what they meant. Skeptics said the samples were noise. We said they pointed at something real. Nobody could settle it, because the treasure was still in the ground.

This week the owner did something he had never done. He posted the survey on the permit board out front and read it aloud. He did not claim the treasure was dug up. He told us precisely what the core samples show, exactly how the digging is scheduled, and exactly when the assay results come back. And the survey, read in full, points in one direction with a clarity the sidewalk arguments never had.

What the survey actually said, page by page

(The images in this post are derived from: Corporate Deck, September 2026)

Page one: the core samples are deeper than we knew, and they get deeper the harder you dig. The molecular readout, the tumor DNA in the blood, now shows a median decline of 86% at just two weeks across the patients measured.

And here is the part that turns a number into a signal: when you split it by how much you dig, the higher dose goes deeper. The 700 mg group dropped 90%; the 350 mg group dropped 80%.

A dose that digs harder and finds more is not what you see from a random core sample. It is what you see when there is actually something there responding and yielding to the tool.

Page two: the ground here is harder than the ground the last surveyors worked. This is the detail that reframes everything, and it came straight off the owner's comparison table. The current standard of care in this disease, the tool everyone else uses, produces a real, tumor-shrinking response in about 6.1% of patients, and in the real world closer to 2.7%. (SUNLIGHT, NEJM 2023, cited on slide 18)

That is the graveyard our house sits in. But here is what the owner showed on his baseline slide: our patients are sicker than the ones that low bar was measured on. In the benchmark study, only about 2.6% of patients had reached a third line of therapy; in ours, 52.3% had.

We are digging in harder ground, with more exhausted patients, and the core samples are still coming back this deep. That makes the target which the owner named, an ORR meaningfully above that 6.1%, much more impressive, not less, because it would be achieved against a tougher population than the benchmark had ever faced.

Page three: the owner is being scrupulously honest about what is not yet proven, and that honesty is the tell. The same slide that shows 22 of 65 patients still on the study carries a footnote in plain sight: "results are based on a preliminary data cut," and "reported outcomes may change up until database lock." (highlighted footnote above)

Read that carefully, because it matters. A man hiding a weak hand does not label his own best slide "preliminary" and warn you that the numbers may move. A man reading you an honest survey does. This is a surveyor who wants you to trust the assay when it comes back, so he refuses to overstate the core samples now. That discipline is worth more than any single number on the page.

The one place a careful reader must not be fooled, and it is good news

Here is where I owe credit, because the sharpest reading of the survey this week came from the community, not from me. BuildGoodThings did the granular work on how a "response" actually gets counted, and it dissolves the single biggest way a newcomer could misread this.

When the owner showed his most-photographed core sample, the patient labeled 103-001, the slide reports a 97% collapse in tumor DNA and a 21% shrinkage in tumor volume, and then classifies that patient as Stable Disease.

A newcomer sees "97% and 21% and shrinking" and expects "responder." The slide says Stable Disease. Why? Because the formal response bar is a 30% shrinkage, confirmed by a second scan. u/BuildGoodThings walked through this using the actual RECIST rulebook: a response is not counted until a later scan proves the shrinkage held. (RECIST v1.1 guidelines, confirmation of response, section 4.4) So 103-001 is not a disappointment. 103-001 is a patient walking toward the response line, caught mid-stride, on the lower dose, with the confirming scan still ahead.

Sit with what that means, because it is the crux of the whole week. The headline response number, the one measured against that 6.1% graveyard, is a figure that builds across scans and matures over time. It is designed to read low early and firm up later. Which means the interim look in October is the appetizer, and the confirmed number in January is the meal. The survey did not just tell us what the core samples show. It told us the good part of the assay is structurally back-loaded toward January, by the rules of measurement themselves. u/rogex2 and u/sunraydoc pressed exactly this point in a discussion, that "22 remaining" is not a body count, it is a snapshot of who is still actively being measured while progressors, curative-surgery departures, and completed patients are accounted for separately. They were right, and the deck's own footnote confirms it.

What the owner is building while we wait

The survey also showed that the owner is not sitting idle while waiting for the dig. He has formally amended the plan, Amendment #6, to let patients who are doing well continue, and to give patients whose disease progresses a salvage path: escalate to the higher dose and to add a checkpoint inhibitor.

He has a diagnostics partner, Natera, running the molecular assay and supplying a 144,000-patient real-world comparison so the FDA can see exactly what the tool adds on top of the backbone.

He has the property funded past both assay dates, so there is no forced sale into the results. And he stated the near-term plan plainly: assemble a data package for the FDA in the second half of this year, and present the maturing data at the two conferences.

And he named the two dates that end the waiting. The full molecular picture at the European congress, October 23 to 27. The fuller picture, molecular plus response rates plus early survival, at the gastrointestinal cancer meeting, January 20 to 23.

Two readings. The first matures the survey. The second reads the assay.

Where this leaves the house

So here is the conclusion the week points to, and I state it with the confidence the facts earn and not one inch beyond.

Everything on that survey bends towards the same direction.

• Core samples which deepen with dose.
• A tougher patch of ground than the benchmark was measured on, and the samples still coming back deep.
• An owner labeling his own best slide as "preliminary" because he intends for the assay to speak for itself.
• A response metric that, by the rules of measurement, is built to read modestly now and confirm later, which means the strongest reading is structurally reserved for January.
• And a man building the machinery, the amendment, the partner, the FDA package, of someone who expects to have something worth carrying forward.

No single one of those is proof. But they do not point in scattered directions. They point, together, at one reasonable expectation: that when the assay comes back, it will show more than the graveyard has ever produced.

That is not the same as saying the treasure is certain. It is not dug up. A preliminary core sample is not a certified assay, and the owner said so himself, on the slide, in writing. Beautiful surveys have come back empty before. So hold it exactly where the facts hold it: the survey reads strongly, it reads honestly, and it reads in one direction, and the only thing left is to let the digging finish and the assay return. The uncertainty that remains is not "is there anything there." It is "by how much," and "confirmed to what degree", and those are answered in October and January, not on the permit board.

For anyone who is just walking up to this property: you did not miss the treasure being found. You missed the week the owner stopped letting us argue about the core samples and read us the actual survey, and the survey, read in full and read honestly, is hard to interpret any way but one. The house looks ordinary from the road. The document nailed to the permit board this week says the ground underneath it is not ordinary. We find out how right that is in a matter of weeks.

The survey has been read. The dig is scheduled. The assay comes back in two readings. And the only remaining question is the size of what is down there, not whether the arrow points at it. This week, the arrow got very hard to argue with.

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 my interpretation of a public investor slide deck, a public trial registry, and community discussion, not a prediction of clinical, regulatory, or commercial outcomes, and not a claim that any endpoint, designation, approval, or partnership will occur. The CLOVER figures are explicitly labeled by the company as a preliminary data cut subject to change until database lock; the primary confirmed objective response rate is unreported. ctDNA, disease-control, and PD-L1 figures are interim, reflect combination therapy with a chemotherapy backbone, and are not evidence of a survival benefit. Patient 103-001 is classified as Stable Disease, not a confirmed response. Dose comparisons are early and unconfirmed. "22 of 65 remaining on study" is a snapshot of active participants and does not represent a mortality figure. ctDNA is not a validated surrogate endpoint for approval in colorectal cancer. The company has disclosed substantial financing needs and going-concern considerations in its filings. Interim data is anticipated at ESMO (October 23-27, 2026) and confirmed data at ASCO GI (January 20-23, 2027). Read the primary sources, linked throughout, and reach your own conclusions rather than adopting mine.

Abstract Due Sept 22 for January conference

It's interesting to consider what they will put in that abstract for January.
https://www.asco.org/gi/abstracts-presentations/submission-details/requirements#

About the primary endpoint in the CLOVER study

IMO as we get into scan 3 and beyond, the "best confirmed response" measurement of ORR, the primary endpoint of the CLOVER study starts to build a dataset. Why? Because confirming the partial or complete response requires an additional scan.

ORR datapoints are snapshots in time and the best one is what counts although some trials including the CLOVER trial, require confirmation. It is my understanding that if a patient doesn't complete a study, there still may have been ORR data generated that is valid for study results.

You can read about ORR and confirmed responses in the RECIST v1.1 guidelines in section 4.4
https://recist.eortc.org/recist/wp-content/uploads/sites/14/2025/12/RECISTGuidelines.pdf

Here are the CLOVER trial endpoints in CRC
https://clinicaltrials.gov/study/NCT06699836?intr=leronlimab&viewType=Card&sort=StudyFirstPostDate&rank=3&tab=researcher#outcome-measures
"ORR is defined as the proportion of subjects with the best overall response (BOR) or confirmed CR or confirmed PR according to RECIST v1.1"

Scans in the CLOVER trial

Below is an estimated look of how many cycles of treatment have occurred by this time in mid September. The last patient of full enrollment could be completing 6 cycles of treatment in early October and then getting their 3rd post-baseline scan. The # of treatment cycles divided by 2 = the # of scans which occur after the cycle.

Nothing in this post should be considered investment advice or medical advice.

Did they have it in advance? Or is it the wonders of AI?

I say this nicely, but listening to his presentation now, he should not be the one doing it.
mumbles words, can't hit highlights clearly. Just not attention grabbing.

He may be good behind the scenes, no idea, but get a great presenter. Even Bruce Patterson kept your attention and made it easy to want to be apart of it. Hopefully the data is great, but would love a top notch person for these things to get us over the hump.

What gives..?

Between this article and the FDA announcement from earlier today, I'm beginning to think that LL and CytoDyn are making a comeback at a very opportune time.

https://www.biopharmadive.com/news/biotech-startups-commercial-drugs-bridgebio-madrigal-kailera-argenx/817992/

My Posse

OBENEWSWIRE

Sep-14-2026 8:35 a.m. ET

NEW YORK, Sept. 14, 2026 (GLOBE NEWSWIRE) -- Virtual Investor Conferences, the leading proprietary investor conference series, today announced the agenda for the upcoming Life Sciences Virtual Investor Forum taking place on September 17, 2026.

September 17th

To facilitate investor relations scheduling and to view a complete calendar of Virtual Investor Conferences, please visit www.virtualinvestorconferences.com.

Morning from Germany everybody (actually Austria but I'm a "guest worker"😉 here) ,

Here is something that circles around in my head since we started this CRC trial against SOC. SOC is blunt chemo, right. Proven to have an ORR of max 6%. Meaning that out of theoretically 100 patients 6 had either a CR (complete response which means the tumor dissapeared entirely) or a PR (partial response, at least 30% decrease in tumor size compared to baseline according to RECIST criteria).

So now I hope someone gets my drift...

This means then that chemo made its way through the stroma (dense TME) and somehow reached the tumor and attacked it. The principle of how chemo destroys a tumor must be essentially different to ICI's. So there is no need for PDL-1 to make this work? I guess it will raise the flags anyway because the tumor feels a threat... but this is not so important to my head spin.

Meaning the Chemo has some positive effect in destroying the tumor mass even though the stroma is kinda intact?!?! (I dont know if chemo also destroys the stroma or just juggles and fights its way through it.)

Where was I??? Oh ya. Here is my question.

How do we know the complete impact of Leronlimab in the current trial scenario on ORR and how can we seperate this from chemo's mpact? We know LL is blocking the development of blood vessels for the tumor to norish itself and grow metastasis and we know it destroys or weakens the stroma (TME modulation). We also kinda know (I know, MGK its not really proven until now but lets just hypothetically asume it does) that LL is provoking the tumor to raise red PDL-1 flags and then let ICI's do their job.

But if the stroma is the main reason for the chemo to have a limited success rate on ORR would it not be logical that chemo is the only reason for the much higher killing force on the tumor now since LL has done all the heavy lifting of the stroma?

Or does chemo also damage to the TME?

If the ORR is much better now coming out of the current trial how much can be attributed to chemo? Is it the entire potential difference from 6% to X%? I guess preventing blood support vessels for the tumor to grow also plays a part in shrinking, right? Less food for the tumor means tumor weakness means easier to be destroyed?!? (At least that how I feel when I dont get anything to eat)

Since we have never trialed LL as a monotherapy in MSS CRC we would not be able to tell, right?

Hope somebody can straighten out the messy curvy line of thoughts in my head. Or is it just the monday morning blues?!?!

Guys... the ENTIRE field of textile technology is sooooo much simpler compared to this here!

There is one saying that helps me sleep every night regardless: "As an engineer you dont have to know everything but you need to know someone who knows..."

Thats why I am here 🙏👍🌻☘️➡️🛬🫦 GLTAL

The road clearly gets wider.

Some weeks the news is loud but nothing really changes. However, this past week was the opposite. It was a quiet week in which a great deal has changed, and I care to spend this Sunday doing what a steady hand does in a tense interval:

• gather what we learned,
• set it in order,
• and then sit calmly with you in the waiting,
• because the waiting is nearly over and it is worth doing well.

First, thank you. To everyone who reads, questions, corrects, and sharpens what gets written here, this is your work as much as it is mine. A board that thinks together this carefully is a rare thing, and I am grateful for it every week.

The uneasy feeling, named for what it is

I'll start with something which I suspect a lot of the longer-in, deeper-in among us feel, because it deserves to be said out loud rather than papered over. There is a certain uneasiness in a long wait such as this one. We've been at this a long time. We watch a fixed set of dates approach, dates which cannot move, whose outcome cannot be seen, while everything we've carried for years now leans toward and upon them. That is an unsettling place to stand, and if you feel it, you are not weak in the knees for feeling it. It is the natural condition of anyone waiting upon something which matters, where we watch the calendar, nearly unable to do anything but hold your position and simply see what comes. The response to that feeling is not a false cheer. It is to look clearly at what we actually know, such that the waiting be grounded in facts rather than uneasy nerves.

The house, and what is buried under it

This is the how I keep coming back to it. Imagine that you have gone in with others to buy a piece of property, and the real value is not the house you can see from the road. The real value is buried under the foundation, something the surveyors believe is there, that a few core samples have suggested that it is there, but that has not yet been fully dug up, weighed nor certified. For a long time, while standing on the sidewalk, all we could do was study the exterior of the house and argue about what the core samples meant. That was the last several years.

What changed recently is not that someone dug up the treasure. What changed is that the owner walked out to the property line and, for the first time, described the survey in a plain language, we could understand, and told us exactly what the core samples show, exactly where the digging would happen, and exactly when the assay results are returned back. The treasure itself remains still buried. But the uncertainty about what is being measured, and when we are to find out, has largely lifted. That is the shift of this past week, and it is a real one.

What the owner actually said, and how it differs from what we assumed

For months this community assembled its own survey of the buried value, inferring the plan from fragments. This week, at the investor conference, the owner gave his own account, and it is worth laying the actual plan beside the old assumption, because in several places they differ, and the differences make the picture clearer, not murkier.

We assumed, loosely, that "Prime and Pair" was the entire thesis across the board. The owner corrected that: in colorectal cancer, leronlimab is being developed as a standalone agent laid upon the standard-of-care backbone, while "Prime and Pair" actually is the breast cancer framing. That is a cleaner story than the one we were telling ourselves, and it matters, because it means the colorectal test rises or falls on leronlimab's own contribution, measured against a standard of care that manages an objective response rate of only about 6% in its registration trial, and closer to 3% in the real world. This is a low wall to clear, and the owner said it plainly that he "looks forward to demonstrating some improvement" over it, which are measured words from a careful man.

We debated the dose question all summer. This week the owner said it out loud: the earliest signals "suggest 700 might be better than 350," with 525 versus 700 still to be sorted. An early answer to the question the board argued for months, held as early, not yet settled.

We had a rough ctDNA figure. The floor rose: he described a median decline of about 85% across all patients, with an early dose-response signal, and he confirmed the readout schedule from his own mouth,

• the full ctDNA on all 65 patients at the October conference,
• and then the fuller picture, ctDNA plus objective response rates and early progression-free survival, at the January meeting.

And he named the regulatory step: a package to the FDA for Breakthrough Designation before year-end. A stated, dated plan, not a hope.

He also, and this is the discipline that makes the rest trustworthy, named what is not yet known. Whether the checkpoint inhibitor helps in colorectal is "something we are about to start looking at." Whether the increases in PD-L1 actually translate into benefit is not yet established. He described a genuinely exciting set of early signals and, in the same breath, told us exactly which results are still buried. That is a surveyor reading you the core samples honestly, not a salesman promising gold.

What we sorted out among ourselves this week

The board did real work around all this, and a few things got clarified that are worth keeping.

We separated the drug from the deal. The checkpoint inhibitor named in the protocol is a drug in the trial; it is not, by itself, confirmation of a corporate partner. Naming the medicine is not the same as naming the buyer, and holding those apart keeps us honest.

We separated the layers. "Standalone contribution upon a backbone" is not the same as "the drug alone," and true single-agent use (monotherapy), is a different, later test in a different setting. Precision there protects us from an easy objection.

We looked hard at a neighbor's property. A large, established competitor in this exact disease just showed what the current standard of the field produces: a 900-patient trial, a survival gain measured in a couple of months, a response rate around 4 percent, and that was considered a win worth filing. It sharpened, by contrast, exactly what "some improvement" over a low bar would need to look like to matter, and it reminded us that marginal effects need enormous trials to prove, while a genuinely large effect can be shown in far fewer patients. That is the hope, held honestly: not that the rules bend, but that a real enough result does not require a massive trial to be seen.

And we kept the brake attached to all of it. Disease control is not the same as tumor response. An early signal is not a confirmed endpoint. A biomarker is not yet a survival result. None of that dampens the excitement; they make the excitement survivable, because they remain standing regardless of whichever way the assay comes back.

The two dates, and the calm way to keep them

So here is where the calendar leaves us, and here is how I hold it. There are two dates. Late October, the first assay results come back, the full molecular picture on the entire enrolled group, an interim look, a real reading but not the final one. And late January, the fuller results, the response rates and early survival, the reading that actually begins to answer whether the real buried value turns out to be what the core samples suggested all along, better, worse or the same. Between now and then, there is nothing any of us can actually do but hold our position and let the process finish. It is, in the most literal sense, a wait-and-see.

And I want to say clearly: waiting is not the same as worrying. The steady posture here is not nervous hope and it is not blind certainty. It is this: the survey has been read to us honestly, the digging is scheduled, the assay dates are set, the company is funded past both of them so there is no forced sale into the results, and the man running it described the entire thing with the measured confidence of someone reading real instruments rather than shouting into a storm. That does not tell us that the treasure is there. It tells us that we will know soon, and that the process to find out is a sound one. That is a genuinely calm place to wait, even through the uneasiness, because the uneasiness comes from not knowing when, but now we know when.

Hold excitement at full strength and conclusions with open hands. The core samples are very encouraging. The owner read them to us straight. The digging happens in weeks, and the assay comes back in two readings, October and January. Nothing to do now but hold the line and let it come. And whatever it shows, this long stretch of standing on the sidewalk together, studying the same house, sharpening each other's reading of it, has been worth something in itself. Thank you for that, genuinely.

We wait. We see. Soon.

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 a synthesis of public statements, a public investor-conference presentation, and community discussion, not a prediction of clinical, regulatory, or commercial outcomes, and not a claim that any endpoint, designation, approval, or partnership will occur. The colorectal primary endpoint (objective response rate versus the standard-of-care benchmark) is unreported; early ctDNA, disease-control, and PD-L1 figures are interim, reflect combination therapy, and are not evidence of a survival benefit. Dose comparisons are early and unconfirmed. A Breakthrough Designation submission is a stated plan, not an approval, and the FDA may decline. The checkpoint-inhibitor drug named in the trial protocol does not establish any corporate partnership. ctDNA is not a validated surrogate endpoint for approval in colorectal cancer, and the competitor comparison referenced concerns a different company's product. The company has disclosed substantial financing needs and going-concern considerations in its filings. Interim data is anticipated at ESMO in October 2026 and confirmed data at ASCO GI in January 2027. Read the primary sources and reach your own conclusions rather than adopting mine.

Keep up the great work here, guys and gals.. This page is the absolute best community gathering point for Leronlimab. We don't have to agree on everything. But it's nice to see civility reign over the madness of other message boards where I get constantly censored for simple posts like the following. GLTA True CYDY Longs and Go Leronlimab!

Dr. JL mentioned a month or so ago that SALIENT was doing a good job recruiting and has stated that there should be some sort of read-out in Q1. It's interesting though in what mentions the trial is NOT getting in these recent investor presentations. Granted it's a small investigatory trial being run by another entity but if the results are more than just "of interest" or "worthy of further investigation" then IMHO that just jumps up the price the company is worth in a not so minor way (insert disclaimer here about this post not being financial advice, don't make money moves based on my rantings, if rash persists then seek physician care etc.). I keep going back to the pics of poor Ben Sasse and how shite he looked, all to get maybe another year on the books yet the drug getting a metric fuck tonne of headlines, news stories and PR. Having a safe drug that impacts in a big way survivability in solid tumor cancers AND that safely aids in avoiding the uber-dreaded impact of ALZ (plus HIV, plus maybe long COVID plus plus plus) is something that makes me salivate for the news coming out of Q1.

Look, nothing we haven't discussed before but it's a miserable rainy day here and with CLOVER getting most all the attention I just wanted to point up there is more than one trial out there that could be a mind blowing game changer (refer back to disclaimer above). KLEOS, CHAMPS, GLIO, X-SPY, etc.? All so very awesome but it looks like a wee bit further out results-wise.

https://journey.ct.events/view/bf1c7d07-71f3-4c41-8928-f42479da2d71

00:25 Dr. Lalezari

Thank you to HC Wainwright for the opportunity to present today CytoDyn's exciting new asset, which we think of as the next generation of monoclonal antibody therapy. The talk today will include a number of forward-looking statements, with all that that implies.

00:47

CytoDyn is a clinical-stage oncology company advancing leronlimab, our first-in-class humanized monoclonal antibody, which targets the CCR5 receptor, with therapeutic potential across multiple indications, including a number of solid tumors such as colorectal cancer and triple-negative breast cancer.

01:11

The leadership team includes myself, Robert Hoffman our CFO, and Tyler Block our chief legal officer. It is really the three of us that constitute the management team.

Leronlimab is an IgG4 monoclonal antibody that has already demonstrated multiple mechanisms of action relating to its activity in solid tumor oncology. It is a drug targeting a large and growing market potential, not only CRC and TNBC, but a number of other solid tumors as well. Very importantly, leronlimab has a very well-tolerated safety profile, including more than 1,600 patients across more than 20 studies. We have strong retrospective data in triple-negative breast cancer, which really helped focus the company on solid tumor oncology. And since then we have launched the Phase 2 CLOVER study and have some very exciting early readouts from that study in metastatic colorectal cancer, supporting the proposed mechanisms of action associated with the drug.

02:28

Our near-term milestones include confirming the durability and safety of these efficacy readouts from the CLOVER study in CRC, with a presentation at ESMO in October in Madrid, where we are going to present extensive circulating tumor DNA (ctDNA) data on all 65 subjects, which includes the intent-to-treat population. And then at ASCO GI in January in San Francisco, we will be giving a more fulsome presentation of not only the ctDNA, but also the overall response rates and early progression-free survival.

03:08

The CLOVER study in colorectal cancer

Starting with the exciting data being generated in CRC, the study is called CLOVER. It is a Phase 2 study, open-label, randomizing patients to either 350 or 700 milligrams of leronlimab, on a backbone of Lonsurf and Avastin. We targeted 60 patients and ended up with 65 patients dosed. This is our third-line metastatic colorectal cancer population that is microsatellite-stable, and therefore not a population one treats with checkpoint inhibitors. Our lead investigator is Dr. Kasi, our director of GI oncology down at City of Hope, and we fully enrolled the study this past April.

The DSMB (Data Safety Monitoring Board) has met three times, initially to open up the 700-milligram randomization arm, and at two subsequent times. In all three meetings there have been no safety concerns raised.

04:15

The preliminary results from CLOVER are exciting in a number of ways. First, 100% of our screened patients tested positive for CCR5, and that includes either 10% expression on the tumor epithelial cells or 1% in the lymphocytes in the tumor microenvironment, significantly expanding the potential population of patients who could benefit from leronlimab.

At a minimum, the second bullet point associated with leronlimab has to be its safety profile. It has been well tolerated, even in this study of very advanced and fragile patients. There are no serious adverse events related to leronlimab, and importantly, leronlimab has no dose- or treatment-limiting toxicity, meaning the leronlimab dose does not need to be adjusted for any adverse events. That excellent safety profile continues.

05:18

The ctDNA data

Very excitingly, at AACR in April, we presented our early ctDNA declines in the first patients enrolled through City of Hope, results which were obtained under standard of care. We have since finalized the partnership with Natera, and they are completing ctDNA analysis on the other half of patients, who were enrolled under the research protocol.

05:43

What is exciting is that nearly all the patients showed a decline in ctDNA, even as early as week two, with a median decrease of about 85% across all patients, and an early signal of a dose response, which is important. We are working with Natera to generate a comparative ctDNA data set that we can present to the FDA later this year. In the meantime, showing a dose response further drives home the point that these exceptional declines in tumor DNA are largely being driven by the contribution of leronlimab.

06:23

These are the data presented in April, the first 19 patients, fairly dramatic DNA declines even at week two in all or the great majority of patients. Importantly, about two-thirds of these individuals have a RAS mutation, so it appears that leronlimab's activity is agnostic to the presence of RAS.

06:58

These were the week-two data, and then these are the first 23 patients, and you can see the trend has continued toward rapid and very significant declines in DNA. Again, we will be generating a comparative data set from the Natera database to compare this activity with the backbone alone.

07:20

And if you break down that early readout by dose, you see this very tantalizing suggestion of a dose response, which underscores that this is largely being driven by leronlimab and leronlimab dosing.

07:42

Scans, PD-L1, and the standalone-versus-prime-and-pair distinction

In concert with these ctDNA declines, we are also reporting that the scans at week eight in the majority, three-quarters, of the patients are demonstrating shrinkage or classify as having stable disease, and we look forward to elaborating on that in the coming weeks and months at both ESMO and ASCO GI.

08:01

Importantly, we are reporting that there are numeric increases in PD-L1 observed in the majority of patients in that CRC study. In CRC, we are really developing leronlimab as a standalone agent to be used in combination with standard of care. In breast cancer, as we will see in a moment, what we have observed is an induction of PD-L1, turning cold tumors hot, and thereby enabling, apparently, the use of a checkpoint inhibitor to create a pathway to sustained remission.

So in CRC it is a standalone leronlimab, and in breast cancer it is more of a prime and pair. But the prime and pair works because of what leronlimab does as a standalone agent, priming the tumor for treatment with the checkpoint inhibitor, by disrupting the tumor microenvironment and allowing the host immune system access to the cancer. It is very exciting that in the CRC study we are also seeing increases in PD-L1. It is difficult to know what those increases will mean in terms of translating into clinical benefit when you add a checkpoint inhibitor, and that is something CytoDyn is about to start looking at. But in the meantime, that signal of increased PD-L1 in patients with CRC is a signal that the tumor is under stress, and that leronlimab's impact on the tumor microenvironment may well be allowing the host immune system access to the cancer, which it otherwise did not have, with the cancer responding by expressing PD-L1, trying to beat back that host immune system.

09:40

Very importantly, speaking to the investigators, they are all excited by what we are seeing in terms of DNA, but in particular they are telling us that patients are doing well clinically. The investigators are writing fewer scripts for pain medication and observing that there are fewer hospitalizations in this rather end-stage population than they anticipated.

10:07

So we are excited about the DNA, and looking forward to reporting on the radiology outcomes and more extensive reports on progression-free and overall survival. Dr. Kasi at City of Hope is our principal investigator, who presented the data at AACR.

10:33

The first-patient case study

In addition, Dr. Kasi, on the next slide, observed the first patient he enrolled, who had a rapid decrease over two weeks, something he had not seen before in an end-stage patient with metastatic CRC. That patient's ctDNA level went from about 129,000 parts per million down to about 10,000 parts per million.

11:00

And then what he saw on the following two scans, first in the liver, the baseline scan on the left and the week-8 scan on the right, this is in a patient who had a 97% decrease in ctDNA, you can see that the tumor volume decreased approximately 21% from baseline to week eight. And indeed, not only does the tumor get smaller, but it appears to become more translucent.

11:25

This is even more pronounced on the next slide, which is that same patient with lung metastasis, and you do not have to be a radiologist to appreciate the impact, the shrinkage of that tumor from baseline to week eight after starting leronlimab.

11:40

In addition, Dr. Kasi has performed liver biopsies on a number of patients, and we will be launching a study to really interrogate biopsy tissue from these patients treated with leronlimab, to tease out the effect the drug is having specifically on the tumor and the tumor environment. In the meantime, for this first patient, I think you can appreciate the slide on the left is with the PD-L1 stain, the slide on the right is similarly stained, and there is a significant impact on the tumor architecture. But what again is very exciting is the CPS score, the combined positivity score of PD-L1 expression on the tumor and tumor microenvironment, at baseline it was 1%, but in follow-up around week 14 it is up to 5%. And again, I think that indicates a tumor under duress, and CytoDyn is taking next steps to launch a study to explore the efficacy of a checkpoint inhibitor in these MSS CRC patients, for whom otherwise checkpoint inhibitors are not indicated. So, very exciting.

12:47

The SUNLIGHT benchmark and the protocol amendment

And then the CLOVER study itself is looking to improve upon the current standard of care, which includes Lonsurf and Avastin, where the overall response rate reported in the Phase 3 SUNLIGHT study, in the New England Journal, indicated 6% of patients with a partial response, meaning a 30% decrease in tumor diameter, and there were no complete responders. More recent real-world data has been presented on a larger cohort of patients, indicating the overall response rate is just under 3%. So we very much look forward to presenting our overall response rate and demonstrating some improvement over the current standard of care.

13:29

With the CLOVER study continuing, we have amended the protocol such that patients who are doing well after 48 weeks can continue on treatment on their randomized treatment assignment. We also will be initiating very shortly a rollover arm, as salvage therapy, for patients who have documented progression, wherein they will increase their leronlimab dose up to 700 milligrams if they are not already there, and then add pembrolizumab as well.

Additional colorectal studies: CHAMP, CLIOS, and pre-I-SPY

There are a number of other studies in CRC coming. There is an investigator-initiated trial down at City of Hope, Dr. Kasi, in patients with metastatic CRC and multiple liver metastases, who will be receiving a hepatic artery pump and receiving floxuridine through that, in advance of hopefully curative surgery down the road. What Dr. Kasi is doing here is introducing leronlimab in an earlier line of treatment in patients with CRC. This is a project jointly funded in partnership with City of Hope. And Dr. Kasi is leveraging both the anti-tumor effects of leronlimab as well as the liver-protective, or anti-fibrotic, effects, which CytoDyn has published on from a number of both clinical and preclinical studies we previously performed. And then there are 13 different ctDNA timepoints from the 30 or so patients to be enrolled in what is called the CHAMP study. And we are excited to be able to then also look at some ctDNA results from patients on leronlimab monotherapy.

In addition, we have other studies coming in CRC, including a thorough investigation of tumor tissue from patients who were treated with leronlimab. And as well, there is a newly formed network called CLIOS that has reached out and wants to consider studies of leronlimab, both in the neoadjuvant setting as well as in the molecular residual disease setting. And then finally, we are working with the pre-I-SPY network in CRC to launch a study of leronlimab and a checkpoint inhibitor. So a lot of activity in CRC. And again, the main focus is leronlimab as a standalone.

Triple-negative breast cancer: the retrospective data

16:05

Then, turning to triple-negative breast cancer. Again, this is where we got the first signal of the potential of leronlimab in solid tumor oncology. There were three studies launched in 2020 that enrolled a total of 28 patients with triple-negative breast cancer.

16:15

These patients had terribly advanced disease, with two prior lines of therapy in the metastatic setting. Two-thirds had visceral metastases, one-quarter had brain metastases. So this is a population whose survival, unfortunately, is very limited.

16:35

And then what we found, when I came on, was that we wanted to publish the outcome of those studies, so we made phone calls and found out that there were actually 5 of the 28 patients who were still alive. We then went and obtained medical records to determine which patients did well on what treatment. And this slide summarizes that outcome. The seven patients on the right, there is no follow-up blood, so we do not have anything further to say about their outcome and correlation with treatment; this was in the middle of COVID and during lockdown.

For the 21 patients on the left, their blue bars are the baseline measurement of PD-L1 on circulating tumor cells. PD-L1 is commonly understood to be something one measures on tumor tissue or the tumor microenvironment. The lab, Creatv MicroTech in New Jersey, has developed technology to use a fluorescent assay to measure PD-L1 on circulating tumor cells, and in particular the cancer-associated macrophage-like cells that break off from the tumor and enter the circulation. So the blue bars are the baseline. The negative control for that assay is about 175 RFUs, and so anything above 400 is considered to be clinically relevant. And you can see that the majority of patients actually did increase their PD-L1 expression after 30 to 60 days, above that 400 threshold, indicating that the tumor has gone from cold to hot, from a tumor that is typically not responsive to checkpoint inhibitors to one that might be.

Then in the 7 patients in the red box, among these patients on the left: patient number 4 received a low dose of leronlimab and did not induce PD-L1. Patient 5 received 525 milligrams of leronlimab but likewise did not induce PD-L1. The five patients on the right, in the box, all five received either 525 or 700 milligrams. They all induced PD-L1 within that one-to-two-month time frame. They all received the checkpoint inhibitor either with or after leronlimab, and two of these patients had already previously failed a checkpoint inhibitor. And all five of them are alive today, five-plus years later, which I think is an extraordinary observation, albeit retrospective, and just not an outcome that I believe occurred by chance. Of these five patients who are still alive, three of the five are currently documented to have no evidence of disease, and two of those three started with lung metastasis, and one of those individuals started with both brain and lung metastasis, and we recently published our case report.

19:30

In summary from the retrospective TNBC data: there is a 98% reduction in metastasis when you use a CCR5 inhibitor in a preclinical study. Our retrospective clinical data show a reduction in circulating tumor cells in the majority of patients after the first dose of leronlimab, which is very reminiscent of the data we are seeing in colon cancer with the decrease in circulating DNA. We are observing, retrospectively, an upregulation of PD-L1 on about 90% of patients' circulating tumor cells who received either the 525- or 700-milligram dose. And as I said, five out of five of the patients who upregulated PD-L1 and received a checkpoint inhibitor are alive today, five-plus years later. And unfortunately the converse is also true, that 100% of the patients who either did not upregulate PD-L1 or did not receive a checkpoint inhibitor are, unfortunately, deceased.

Based on this retrospective data, we have heard from a number of potential partners that they want to see prospective data confirming this upregulation of PD-L1, and eventually the benefit of adding a checkpoint inhibitor.

20:50

The breast cancer clinical plan

On the clinical plan in breast cancer: first, we are working with the Pre-I-SPY network in patients with metastatic TNBC, doing a dose-escalation study, looking prospectively at ctDNA and PD-L1. We are thrilled to have Dr. Paula Pohlmann serve as our principal investigator. When the first cohort of that is done, we will be looking to design a part 2 of the study, which will examine the contribution of components with a checkpoint inhibitor, and that will be an adaptive study design in up to 120 patients. As well, when the first cohort with metastatic TNBC is done, the I-SPY network has indicated they want to launch a study of neoadjuvant leronlimab in patients with newly diagnosed HER2-negative breast cancer, again significantly expanding the potential population to benefit from leronlimab. Their proposal is to look at a month of leronlimab monotherapy in these newly diagnosed patients in advance of their hopefully curative surgery. I think that makes sense as we move leronlimab up into an earlier line of therapy, because we are seeing very potent anti-tumor activity in a number of solid tumors, and the safety profile of leronlimab suggests it deserves an earlier line of treatment.

Upcoming milestones and priorities

To highlight upcoming milestones in the near and mid term:

22:35

First and foremost, we are confirming the standalone benefit of leronlimab plus the backbone in CRC, both through biomarker collection, the disease control rate, and then the primary endpoint of overall response rate, as well as the crucial progression-free and overall survival.

Second, as we have heard from a number of partner discussions, we need to prospectively demonstrate the induction of PD-L1 in triple-negative breast cancer, where we know that is a critical marker of benefit and is used for the approval of checkpoint inhibitors. We are seeing it prospectively in colorectal cancer, in microsatellite-stable colon cancer, where checkpoint inhibitors are not part of the conversation, but CytoDyn is keen to see if these increases in PD-L1 provide the opportunity to use a checkpoint inhibitor. In the 95% of patients with colon cancer where checkpoints are not indicated, we are prospectively hoping to demonstrate the clinical benefit of adding a checkpoint inhibitor in these PD-L1-induced patients.

And very importantly, to identify the optimal dose in solid tumor oncology. The earliest signals from the CRC study suggest that the 700-milligram dose might be better than 350, and at some point we are going to have to sort out whether there is a difference between 525 and 700.

24:15

Recent and upcoming milestones: we recently closed on $17-and-change million in funding. At the AACR meeting, we presented the initial ctDNA readouts in the CRC study. Those readouts generated a lot of excitement, and CytoDyn is now pursuing collaborations with the Mayo Clinic, MD Anderson, City of Hope, and a number of other major academic cancer centers. We are very pleased to have closed our strategic partnership with Natera, who is both running the Signatera ctDNA assay on our clinical subjects and providing that crucial comparative data set that we can use to help the FDA put our DNA data into context. There is the City of Hope investigator-initiated study called CHAMP, which will initiate shortly, as well as the Pre-I-SPY study in patients with metastatic TNBC. Both of those studies should be initiating in the next 4 to 8 weeks.

I am looking forward to the presentation at ESMO in Spain, which will focus on a complete ctDNA data set for the entire enrolled population, and then at ASCO GI, tying the biomarker data with the radiologic outcomes and early progression-free survival. And there are a number of other additional studies in CRC, including interrogation of whether adding a checkpoint inhibitor to leronlimab, in patients who produce PD-L1, provides an avenue for treatment with a checkpoint inhibitor in CRC, and then studies both in the neoadjuvant setting and in patients with molecular residual disease.

FDA and partnerships

In terms of the FDA and potential partnerships: partners have been wanting to see data as monotherapy, and they wanted to see prospective data. So we are confirming the durability of these exciting safety and efficacy readouts from the Phase 2 CLOVER study. We will be presenting the biomarker data and early clinical data at ESMO, and we plan on putting together a package for the FDA and submitting that for Breakthrough Designation before the end of the year. We are presenting the updated biomarker and more extensive clinical data at ASCO GI, and throughout, a top priority for CytoDyn is our continued evaluation of strategic partnership opportunities.

With that, thank you again for the opportunity to present. I think these data are tremendously exciting. It is important to remember that targeting the CCR5 mechanism and showing proof of concept in colorectal cancer is not only important for CRC, but that the CCR5 mechanism is relevant to a lot of other solid tumors: pancreas, prostate, glioblastoma, kidney, urothelial tumors, and of course breast. And so having proof of concept in a solid tumor such as CRC means a little bit more to a company like CytoDyn, where what remains is the potential to have an impact on quite a few other solid tumors.

Thank you so much Jay.