In the Cup of Trembling, I wrote about who waits and who chooses, and about a pearl buried under the foundation of the house. This post is about the thing the entire house is built toward, and the word for it is one I have used before on this board and have come back to because nothing else fits. Convergence. Not a coincidence of events. A set of separate roads that always were, if you trace them far enough, headed for the same intersection.

Before I show you how the roads converge, I want to ask the question underneath all of it, because the answer is the compass for everything which follows. What is pharmacotherapy actually for? Why do drugs exist, and why does the system approve the ones it approves?

What a drug is for, and why that question decides everything

Strip away the stock, the partners, the tape, and what is left? A drug exists for one reason: to change the course of a disease in a human being who would otherwise suffer it. That is the entire purpose. Everything else, the trials, the endpoints, the approvals, is machinery built to help us answer one question with sufficient certainty to act upon: does this thing actually help a person, and is it safe enough to be worth it.

That is not my framing. It is the law. To approve a drug, the FDA requires what the Food, Drug, and Cosmetic Act calls substantial evidence of effectiveness, drawn from adequate and well-controlled investigations, weighed against safety. (FDA, providing clinical evidence of effectiveness) The system was built, deliberately, to be unmoved by any mechanism which sounds good, by stories, or by conviction. It wants proof that the path of disease bent. In recent years the agency has even formalized a path where a single convincing trial plus confirmatory evidence would suffice, which lowers the number of trials but not the standard of proof.

Keep that, because it is the discipline which makes convergence meaningful rather than wishful. Convergence only counts if the roads converge on that, on proof that a disease is bent in a human being. A dozen roads which converge on a nice idea converge on nothing. So as I lay out the roads, watch where they together meet, and watch whether they meet at the one place the law says actually matters.

Road one: the molecule was never built for one disease

Two years ago I wrote that leronlimab would lift the response rate in colorectal cancer, and I graded that post plainly in my last writeup, right structure, wrong specifics, a number I felt rather than derived. But underneath the specifics which I got wrong, was a structure I got right, and it is the first road. Leronlimab blocks CCR5, and CCR5 is not a colorectal receptor. It is a chemokine receptor that the published literature places at a crossroads the body uses in cancer after cancer, after cancer. The AACR review in Cancer Research surveys CCR5 as a broad oncology target across tumor types, not a single-indication one. (Recent Advances Targeting CCR5 for Cancer, Cancer Research 2019)

https://preview.redd.it/ao3pg17tptuh1.png?width=702&format=png&auto=webp&s=490acf3559c1257b774e8637b43788e3bdb48725

In breast cancer, the published work shows leronlimab blocks metastasis and sharpens the killing done by DNA-damaging chemotherapy. A 2026 review places the CCR5-CCL5 axis upstream in pancreatic cancer alongside the other lethal solid tumors, naming leronlimab's translational potential directly.

So the first road is the molecule itself. The literature describes a multi-use key, not a single-door tool. That is road one, and it is laid down in the journals long before any of us arrived.

Road two: the history of what happens when a key is recognized

The second road is not biology, it is precedent, and it is the reason the first road matters commercially rather than only scientifically. There is a documented pattern in modern medicine for what happens to a drug the day the field stops seeing one disease and starts seeing a mechanism which spans many.

Pembrolizumab, Keytruda, was approved in September 2014 for one thing, advanced melanoma that had failed other therapy. (Merck, first FDA approval of KEYTRUDA, 2014) It was not a melanoma drug any more than CCR5 is a colorectal receptor; it released a brake the immune system puts on itself, and that brake is universal. In May 2017 the FDA approved it for any solid tumor carrying a molecular signature regardless of where the tumor sat, the first tissue-agnostic approval in history, the day the field officially stopped seeing a disease and started seeing a key. Keytruda now carries roughly forty indications and is the best-selling drug on earth. The molecule never changed. The recognition changed, and the value lagged the recognition.

Road two is the map of road one's destination. It tells us what a recognized platform is worth, and it tells us the recognition is earned at a specific place: the first confirming clinical proof, then the second that shows the key fits a distant lock.

Road three: the trial that turns the key, in the open, right now

The third road is CLOVER, and this is where the two abstract roads touch ground. CLOVER is the first door, metastatic colorectal cancer, the setting where the response rate either proves the key turns or does not. CytoDyn presents updated CLOVER data as poster 820P at ESMO on October 25, presented by Dr. Benjamin Weinberg of Georgetown, with the abstract released October 19. (CytoDyn to present CLOVER data at ESMO 2026) That is the sound of the key going into the lock. ASCO GI in January, the confirmed response rate, is whether it turns.

And behind that first door, the other doors are being cut in the open, which is the part that makes this convergence not a single bet. The pre-I-SPY platform was amended to pan-solid-tumor. The CHAMP study takes a liver biopsy. The breast program carries the pooled survival signal that a 2026 review summarized as median progression-free survival around 6.1 months and overall survival beyond twelve, with the longest follow-ups past thirty-six months in some cases. Those are some of the other locks, pre-cut, waiting to see whether the key which turns in colorectal is the universal, master key the CCR5 literature says it should be.

Where the roads meet

Now stand back and look at the intersection, because this is the whole post.

Road one says the molecule is a key, in the journals. Road two says a recognized key is repriced like a city, in the regulatory record. Road three says the proof that converts the key from recognized to demonstrated is being generated right now, on a schedule, in the open. And underneath all three sits the question I opened with: a drug exists to bend a disease in a human, and the law approves it only on proof that it did. That is the intersection. Every road in this story is converging on a single confirmed clinical result, because that result is the only thing which satisfies all three roads at once. It proves the molecule bends the disease, which is what the law requires. It delivers the first confirming proof, which is what road two says triggers Platform recognition. And it is the readout road three is built to produce.

This is why I keep coming back to the word convergence. It is not that many good things are happening at once. It is that many separated things, the biology, the precedent, the trial, the regulatory standard, all require and depend upon, the same event to resolve, and that event is weeks and then months away. They have been traveling toward it the whole time.

What this does and does not promise

I graded myself two years ago for writing the best case as the only case, so I will not do it here. Convergence is not a guarantee that the roads actually meet in triumph. It is a statement that they meet, and that the meeting point is a single readout that can go more than just one way.

If CLOVER confirms a response rate that clears the backbone, all three roads arrive together: the molecule is shown to bend the disease, the first lock turns, and every pre-cut door becomes a question of when rather than whether. That is the convergence the literature and the precedent point toward, and it is the outcome I lean to. If the readout is muddy, the roads are still real but the meeting together is delayed, and the market's patience, and the company's, gets tested. And if the response does not come, then the key was not what the journals suggested, and we will have learned that at the one place the law says we must, in proof rather than in hope. A convergence that cannot name that third outcome is not analysis, it is a wish with references.

But here is what the convergence does promise, and it is not small. It promises that this was never a lottery ticket on just one disease. It is a mechanism the literature already recognizes as broad, standing at its first door, with the other doors being cut and waiting, moving toward the single kind of proof that the entire apparatus of medicine, scientific, commercial, and legal, is built to recognize. The market is currently pricing a locksmith with just one uncertain door. The convergence of these roads describes a master key at the moment before the first turn. Those two descriptions cannot both survive over the next few months. One of them resolves, at the intersection, in the direction the data points.

We are weeks from Madrid, and a few months from San Francisco. Everything I have documented for years, and everything this board has built in the stretch since, has been traveling toward that intersection. Let us stand at it clear-eyed, remembering what a drug is for and what the law demands as proof, and let the readout, not any of us, tell us whether the roads arrived.

Disclaimer: I am not a financial advisor and nothing here is investment advice. I hold a position in the company discussed and you should weigh what I write accordingly. This post synthesizes published biology, regulatory standards, the documented history of platform drugs such as pembrolizumab, and the current status of the CLOVER trial; the historical and biological claims are cited to primary and peer-reviewed sources above, which you should read for yourself. The convergence described is a framework for thinking, not a promise of outcome. Leronlimab has not received the confirmatory clinical readout the argument turns on; CLOVER data will be presented at ESMO on October 25, 2026, and the confirmed response rate is expected at ASCO GI in January 2027, neither of which has been reported. The pooled mTNBC survival figures are drawn from a published review of earlier studies and are not a prospective result in colorectal cancer. A mechanism recognized as broad in the literature does not guarantee clinical success in any indication, and drugs that make elegant biological sense fail in trials routinely. This one may. Read the linked sources and reach your own conclusions rather than adopting mine.

Proxy’s out. Here’s where I land and why.

FOR — Dunlap and Ndhlovu

WITHHOLD — Urbach, Simes, Brunke

AGAINST — executive compensation

FOR — CBIZ as auditor

The three withheld directors sit on the compensation committee. I support Lalezari and Hoffman. Supporting management doesn’t mean rubber-stamping every pay decision.

We’re still waiting for convincing clinical results. I want additional rewards tied more closely to those results before signing off on more bonuses.

Vote by November 19. Your shares, your voice.

— Vyrologix

I was golfing at my club today and met a microbiologist who had worked with Dr. Jonah Sacha with the Leronimab studies. She’s a member of my club. She had recently retired but was excited about the CR5 receptor. Her lab was right next to Dr. Sacha and was a good friend of his. She felt the only drawback to the molecule was that since it was derived from mice and in human studies she wasn’t sure how long term it would be effective, but said so far it had been a very impressive drug. I’m planning on playing with her and her husband. A very nice lady.

u/MGK_2's post earlier today The Convergence... really hit home with me. The idea that all of these innate biological processes that are within everyone of us, and our ancestors for thousands of years, and we are just now beginning to somewhat understand their mechanisms of actions.

What a complex system the human body is. Some say a miracle, others say millions of years of biological trial and error. I for one believe in the biology.

Another byway heading to the Convergence is the little talked about trial SALIENT AD in Alzheimer's led by Dr. Tracy Butler of Weill Cornell Medicine.
The first patient was dosed with 700mg of LL on June 11, 2026, now over 17 weeks ago.
Trial protocol calls for a 12 week treatment period receiving weekly leronlimab doses, then concludes with a 4 week post treatment evaluation phase. 16 weeks.

Thanks to u/AssociationOdd9941 for The Cornell/Donner Connection: Why the Alzheimer’s Trial (SALIENT-AD) is the Ultimate De-Risking Event for Leronlimab

Dr. Jay now has the data from this first patient in hand.
If leronlimab were a city, it would be Rome.
All roads lead to Rome.

Dear Longs,

I realize how tough it is to endure a stagnant stock price. Our expectations are lofty—and justifiably so. We want to break things, go outside and scream, and, in my case, pull out what little hair I have left on my head. Not much is left to pull!!

What helps me is the conventional path CYDY leadership has chosen to follow. First, you clean up your own house, and we all know how long that took. Then you establish a clear direction. In CYDY’s case, that means prospectively demonstrating that leronlimab works in solid tumors.

I get that we’ve had a few side roads with MASH and inflammation, but we are moving forward in the solid-tumor space. CYDY has improved its financial position by renegotiating obligations with Samsung and Fife and raising money that, according to leadership, should provide runway through August 2027.

They have also introduced LL and its mechanism of action to academic institutions, allowing us to keep other irons hot while moving CLOVER forward. Institutions such as Cornell, MD Anderson, and Mayo have been discussed in connection with this work, including Cornell’s Alzheimer’s trial and other efforts moving through institutional review. The patent portfolio continues to develop, and I believe parts of it could provide a meaningful moat.

But what gives me the most satisfaction—and CALMS my emotions—is the information we’ve received about CLOVER.

I want to make sure everyone understands why a reduction in ctDNA matters, even this early. I am certainly not the first to discuss it. MGK, Twinter, BGT, rogex2, Lab Monkey, Lopside Roof, my69z, and a host of others have dug deeply into this topic. Yet I still see confusion among longs about what these results do—and don’t—tell us.

The key takeaway is this: CLOVER’s reported two-week ctDNA decline is encouraging because published metastatic colorectal cancer research shows that early reductions can precede and correlate with later tumor response. Its importance will become clearer when those early blood-test changes are linked to sustained responses, scans, and survival in the same patients.

That is why I see the anticipated ESMO presentation on October 25, 2026, followed by ASCO-GI, as an opportunity to begin establishing a TREND LINE.

My understanding is that the ESMO presentation will focus on two-week biomarker data. We should be careful about assuming what scans or other results will be available. A molecular response can emerge before a change becomes measurable on imaging, which is part of what makes ctDNA interesting.

If we see encouraging changes after ONLY TWO WEEKS, that will be worth paying attention to. But we also need to keep our terminology straight: the roughly 30% tumor-shrinkage criterion used to define a partial response is different from the overall response rate, which measures the proportion of patients who respond. Neither should be casually assumed from an early ctDNA result. More importantly, molecular changes are unseen through a visual assessment of a scan. Whatever scan results that are reported after two weeks will be remarkable for only two weeks but I am not going to fret over ORR, Partial response or stable response until we get more mature data.

What I hope scientists at ESMO walk away asking is: “These early results are remarkable for only two weeks. What will longer follow-up look like in these same patients?” The results across the two dose groups could make that question even more interesting.

Based on the published ctDNA research, I am optimistic that more mature data will trend in the right direction. I hope the anticipated ASCO-GI presentation in January 2027 gives us substantially longer follow-up, potentially including 24-week results for some patients. The actual follow-up will depend on enrollment dates and the presentation’s data cutoff. BGT has offered a more detailed discussion of that timeline, but that level of detail is not the purpose of this post.

I am sharing why this process helps me stay grounded. Clean up the company. Establish a clear clinical direction. Fund the work. Generate data. Present it. Build on it.

That is the conventional playbook successful companies follow. In my view, CYDY is working through that playbook. It doesn’t guarantee success, but it gives us concrete progress to evaluate.

There are two things CYDY cannot control: how patients ultimately respond to LL and what the stock does from day to day.

Some days, it sure FEELS like somebody is “F”ing with this stock. But the market’s daily nonsense does not determine what LL does in a patient. That battle is being fought in the trenches against mCRC, and I remain highly confident in LL’s potential.

Another post I appreciated was from ibelieveinCYDY, discussing what it could mean if a patient improves enough to become a candidate for surgical resection. Becoming eligible for surgery could be an encouraging clinical development. How that patient’s outcomes are counted, however, depends on the study protocol and its prespecified analysis. But, from what Ibelievein cydy discovered; was very promising and favorabe to the CLOVER data.

I can’t remember exactly where we heard it—I think it was one of the Paulson presentations—but I recall Dr. JL saying that a patient was doing well enough to become a candidate for tumor resection. We don’t know how often that may have happened, and I don’t want to turn one reported example into a claim about the entire trial. Still, that is the kind of development that gets my attention.

These are patients facing very difficult disease. I believe CLOVER has the potential to produce results that compare favorably with SUNLIGHT. Personally, I hope we beat the pants off it. But comparing separate trials requires care, particularly when patient populations and prior treatments differ. The CLOVER data will have to make that case.And CLOVER HAS A VERY STRONG ARGUEMENT. Our Cohort of patients is SIGNIFICANTLY more challenging.

As we know, CLOVER is OPEN LABEL. That gives the investigators and company visibility into treatment assignments and accumulating results, although we should not assume how frequently leadership reviews the data. It also creates the possibility that potential partners could review more detailed information through appropriate confidential discussions, subject to applicable obligations.

Now, I am making a BIG assumption here, but I think it is worth explaining my thinking.

If the ongoing accumulating data are compelling, CYDY could have more mature information available for potential partners than the early results presented publicly at ESMO. I would hope leadership is arranging meetings with companies it has already spoken with.

Leadership has also described feedback from two Big Pharma companies along the lines of: “See how far leronlimab can go without an ICI.” If I have understood those comments correctly, that makes the developing CLOVER results particularly relevant to those conversations. Those two BP's I would think would be sitting in separate hotel suites anxiously awaiting an update on CLOVER.

The public presentation in Madrid may give us an early snapshot. What interests me a lot more is the possibility of private discussions about more mature interim results.

I would LOVE to be a fly on the wall in those meeting rooms.

To be clear, I don’t know whether those meetings are scheduled, what data might be shared, or whether any company is ready to act. That is my speculation. But if continued treatment produces stronger clinical outcomes alongside those early ctDNA reductions, I can certainly see why a potential partner would want a closer look.

Will there be enough evidence for a SMART Big Pharma company to make a move before the world sees more mature results at ASCO-GI in January 2027?

I FREAKING HOPE SO! Why would a BP want to let paradigm shifting CLOVER data become public at ASCO-GI and let other BPs to become competitive with the current discussions. NO WAY, would I want to bring in more competitors.

For now, I am watching the clinical progress and reminding myself why I invested. The stock price tests our patience. The data will test our thesis.

Take a BIG breath in, and let it out.

I believe we’re gonna be ALRIGHT!!

Have a GREAT WEEKEND!

For the life of me, I cannot understand how the share price can be stuck here in the doldrums when, IMO, the doors are about to be blown open. I have been burned with owning this stock during the past 6-7 years, using the fall for massive tax loss harvesting twice. Subsequently I have loaded up by buying more than double the shares I ever had previously. Now I have a cost basis of just over 0.20 and I am finding it difficult to justify increasing my investment beyond the current 20-30% of my portfolio.

Part of me wants the price to get down to more of those extreme lows so I can justify buying more. But, I really don't want to see that happen again because it is painful to watch. Like many here I am fatigued with the waiting for success and anxious with concern for what malfeasance or pranks the competition might try to play as we near the goal line.

USPTO allows 5 extensions on a trademark. Each extension has a life of 6 months. The last extension, number 4 , was granted in July. Better get a moving.

This doesn't mean that anyone else can start using it. It applies only to the name 'Livimmune'. The worst that would happen is we may need to change the name of this board. 😂 (just kidding!)

This is what AI had to say about this.

The Livimmune trademark expiring (or running out of extensions) does not allow any other company to use, manufacture, or run clinical trials with leronlimab. A trademark has nothing to do with drug patents, regulatory exclusivity, or manufacturing rights. It only protects the brand name.

Below is the clear breakdown, grounded in the USPTO record for LIVIMMUNE.

✔ What the 7‑month trademark deadline actually means

The USPTO shows LIVIMMUNE is in “Fourth Extension – Granted” status under an Intent‑to‑Use application.
This means:

• Cytodyn has not yet proven commercial use of the trademark.
• They have been granted multiple 6‑month extensions.
• They have about 7 months left to either:
  • Show actual commercial use of the name LIVIMMUNE, or
  • Request another extension (if eligible), or
  • Let the trademark application go abandoned.

If the trademark lapses, only the brand name is affected.
It does not affect ownership of leronlimab as a molecule.

✔ Can another company start using the name “Livimmune”?

Not while the trademark application is active.
If Cytodyn fails to show use and the application becomes abandoned, then another company could theoretically file for the trademark “Livimmune.”

But this would only give them rights to the name, not the drug.

✔ Can another company start using leronlimab in clinical trials?

No.
A trademark expiration does not give anyone rights to:

• The molecule (leronlimab)
• The underlying patents
• The FDA IND (Investigational New Drug) authorization
• The clinical data package
• The manufacturing process

To run clinical trials on leronlimab, a company must have:

1. Patent rights or a license
2. Control of the IND
3. Access to the drug substance and drug product
4. CMC (chemistry, manufacturing, controls) documentation

None of these are affected by a trademark.

✔ Can another company start manufacturing leronlimab?

No — not legally.
Manufacturing a biologic like leronlimab requires:

• Patent rights
• Trade‑secret manufacturing know‑how
• FDA‑approved facilities
• Access to the proprietary cell line
• Regulatory documentation

Even if the trademark expires, the cell line and manufacturing process remain protected as trade secrets, and the patents remain in force until their expiration dates.

✔ Why trademarks don’t matter for drug ownership

A drug can be sold under many names (brand, generic, internal code).
The trademark only protects the marketing name.

Examples:

• “Keytruda” is a trademark; pembrolizumab is the drug.
• “Livimmune” is a trademark; leronlimab is the drug.

Losing the trademark does not allow anyone else to make pembrolizumab — or leronlimab.

🧭 Bottom line

• The 7‑month trademark clock only affects the name LIVIMMUNE, not leronlimab itself.
• No other company can legally run trials or manufacture leronlimab without Cytodyn’s patents, IND, and proprietary manufacturing rights.
• If the trademark lapses, another company could only take the name, which is meaningless without the drug.

Voted tonight. Yes. Gltal

The historical account of what originally drove Dr. Crohn to dedicate his life to medicine centers on this relationship:

The Origin of the Quest

Growing up in New York City as one of 12 children in an immigrant family, young Burrill Crohn watched his father, Theodore Crohn, suffer constantly from severe, agonizing indigestion and terrible digestion problems. At the time, medical science had very little understanding of chronic gastrointestinal disorders, and his father could find no lasting relief.

Deeply affected by his father's daily struggle, Burrill made a personal vow to study medicine specifically to understand and cure his father’s stomach ailments.

The Accidental Legacy

This filial devotion drove him to graduate from Columbia University's College of Physicians and Surgeons in 1907. He spent decades tracking down the root causes of abdominal pain and chronic inflammation, eventually co-publishing the landmark 1932 paper at Mount Sinai Hospital that defined "regional ileitis"—the condition the medical world chose to permanently name Crohn's disease.

The Generational Twist

While Dr. Crohn went into medicine to save his father, an extraordinary multi-generational loop exists regarding his family and the science of the CCR5 receptor.

Dr. Crohn’s great-nephew, Stephen Lyon Crohn, became famous in modern virology as "The Man Who Can't Catch AIDS." Stephen inherited a rare homozygous CCR5-Delta 32 genetic mutation. Because his white blood cells lacked a functional CCR5 receptor, the HIV virus was physically locked out and completely unable to infiltrate his immune system.

The family name that began with a son trying to solve his father's gut inflammation ultimately became a bridge to understanding how blocking the CCR5 traffic engine can immunologically lock down viral infiltration and systemic tissue architecture.

CYTODYN INC.

2026 Annual Meeting

To be held Friday, November 20, 2026

Voted

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AI places an sp valuation post one indiacation approval at $4 per share assuming a $500m revenue stream and a $100+ Billion valuation for a $30B revenue stream.. So, excepting a BO offer with one approval and several maybe approvals down the line presents an interesting challenge JL regarding when to except an offer and how do you place valuation on expected revenue or in the case of Merck it may not be just a revenue issue. It may be a save the company issue...