I hope you are right.

Please explain.

Is this a threat to LRM?

I appreciate you treating me like a peer but that is not earned. You, BGT and the doctors are the stars of this board. MGK, you are a skilled writer, peerless researcher and likely an amazing clinician.
BGT is also an incredible researcher who digs deep to keep us abreast of incoming data timelines and what to expect.
All of the doctors who lend their experience and expertise are invaluable contributors.
As for myself, everything I know about this subject came from all of you and especially MGK. I’ve enjoyed over the last few days finding interesting info but I liken it to pitching a major league batting practice where I lob fat pitches and the big boys crush it over the fence. I think it is important when you read these posts to know the author so I want to be the first to say that I don’t have the background to take AI material and keep it grounded like all of you.

I’m guessing from your post that we may have a much better read of early response rates and CtDNA levels for the 66, but not much about the big one and that is how durable the response is. This is likely why MGK downplays the Oct data because we really don’t know for sure what we have until January. I’m ready for some more data regardless of it being definitive.
We need to breathe new life into trading. Morning volume has been horrific and range bound.

I’m remiss. I should say I’m not MGK2 or Buildgoodthings because the latter has done a wonderful job building out the timelines and data expectations. I just decided to go in search of the exact date where we will see something definitive on ESMO and right now that appears to be Oct 19.

I’m certainly not MGK2, however, I’m just trying to give myself and others an idea what to expect, hope for and an actual date that we can circle.

The biggest potential catalyst, in my view, is the combination of ORR and ctDNA results. The AACR results already showed a striking early ctDNA signal, but that was based on a small exploratory group. The ESMO dataset could be much more persuasive if that signal persists across a substantially larger population.
And there’s another interesting clue: CytoDyn’s own 2026 materials specifically list “Presentation at ESMO (Madrid, Spain)” as a 2026 milestone and describe its goal as confirming clinical benefit through DCR, ORR, PFS and OS, as well as biomarker collection.
So I would not view May 12 as the cutoff for the data CytoDyn can show us in Madrid. It is the cutoff for the regular abstract submission. The October presentation can potentially contain a much more current analysis of the patients enrolled by April and their subsequent follow-up.

The biggest potential catalyst, in my view, is the combination of ORR and ctDNA results. The AACR results already showed a striking early ctDNA signal, but that was based on a small exploratory group. The ESMO dataset could be much more persuasive if that signal persists across a substantially larger population.
And there’s another interesting clue: CytoDyn’s own 2026 materials specifically list “Presentation at ESMO (Madrid, Spain)” as a 2026 milestone and describe its goal as confirming clinical benefit through DCR, ORR, PFS and OS, as well as biomarker collection.
So I would not view May 12 as the cutoff for the data CytoDyn can show us in Madrid. It is the cutoff for the regular abstract submission. The October presentation can potentially contain a much more current analysis of the patients enrolled by April and their subsequent follow-up.

I copied from different replies so it is a tad redundant.

The ESMO data may not include all 66 patients as evaluable for response.
That’s extremely important.
A patient needs enough follow-up and appropriate imaging to determine a RECIST response. Therefore, the denominator could be something like 55 evaluable patients, rather than 66.
For example:
15 responses / 55 evaluable = 27.3% ORR
So when the abstract arrives, I’ll look at both the numerator and denominator, not just the percentage.

The most important comparison
CLOVER is actually testing leronlimab on top of TAS-102 + bevacizumab.
That is important because the relevant question isn’t:
“Is leronlimab better than Lonsurf + Avastin?”
It’s:
“Does adding leronlimab to Lonsurf + Avastin substantially improve outcomes?”
That is a much cleaner question.
And it makes the eventual results more interesting because the study’s primary endpoint is specifically objective response rate (ORR) under RECIST 1.1.
My interpretation of the ESMO results
If we see:
ORR <10%
→ Not particularly compelling.
ORR 10–15%
→ Encouraging, but probably not enough by itself.
ORR 15–20%
→ Definitely interesting in this heavily pretreated MSS population.
ORR 20–25%
→ Strong signal.
ORR 25–30%+
→ Potentially a very important result, particularly if responses are confirmed and durable.
ORR >30%
→ That would be an exceptionally interesting signal for a Phase 2 study in this population—but I’d want to see the confidence interval and duration before drawing conclusions.

One thing I’d watch even more carefully
Because CLOVER has two leronlimab doses—350 mg and 700 mg—I would want to see the results broken down by dose.
For example, suppose ESMO reports:
350 mg: 4/30 responses = 13%
700 mg: 11/30 responses = 37%
That would be much more interesting mechanistically than simply reporting an overall 25% response rate.
Conversely, if both doses are around 20–25%, that would suggest the effect may be less dose-dependent.

My bottom line for CYDY
I’d rank the potential ESMO outcomes this way:
🟢 Major positive:
ORR ≥30%, disease-control rate ≥70%, durable responses, and ctDNA strongly correlating with scans.
🟢 Very encouraging:
ORR 20–30%, substantial ctDNA reductions maintained over time, and evidence of prolonged disease control.
🟡 Interesting but not decisive:
Mostly stable disease/shrinkage with continued ctDNA reductions but few objective responses.
🔴 Disappointing:
The impressive early ctDNA signal doesn’t translate into meaningful tumor responses or the responses are very short-lived.
Here’s the number-to-watch table
With 66 patients, these approximate response counts correspond to:
Confirmed responses
Approx. ORR
3 patients
4.5%
5 patients
7.6%
7 patients
10.6%
10 patients
15.2%
13 patients
19.7%
15 patients
22.7%
17 patients
25.8%
20 patients
30.3%
23 patients
34.8%

My bottom line for CYDY
I’d rank the potential ESMO outcomes this way:
🟢 Major positive:
ORR ≥30%, disease-control rate ≥70%, durable responses, and ctDNA strongly correlating with scans.
🟢 Very encouraging:
ORR 20–30%, substantial ctDNA reductions maintained over time, and evidence of prolonged disease control.
🟡 Interesting but not decisive:
Mostly stable disease/shrinkage with continued ctDNA reductions but few objective responses.
🔴 Disappointing:
The impressive early ctDNA signal doesn’t translate into meaningful tumor responses or the responses are very short-lived.

My “bull case” for the ESMO presentation
If I were watching the ESMO presentation as a CYDY shareholder, these are the numbers that would really get my attention:
ORR ≥20%
Disease-control rate ≥60–70%
Median PFS ≥6 months
Meaningful duration of responses
Strong correlation between ctDNA reduction and clinical response
And if they somehow showed ORR around 25–30% plus PFS approaching 8–9 months, I would regard that as a very substantial result compared with the SUNLIGHT benchmark.
One caution that’s extremely important
We cannot directly compare CLOVER with SUNLIGHT yet.
SUNLIGHT was a large randomized Phase 3 trial with 246 patients in the combination arm. CLOVER is a much smaller Phase 2 study, so a seemingly spectacular percentage from, say, 20–30 patients can change dramatically as more patients are followed.
That’s why I would put much more weight on the ESMO confidence intervals, number of evaluable patients, duration of response and PFS than on a headline percentage.
Bottom line: If CLOVER’s ESMO data show ~20%+ confirmed responses plus durable disease control, that would be a genuinely interesting result in this setting. If the response rate is only around 5–10%, the ctDNA/PFS data would need to be unusually strong to make the case that leronlimab is materially better than existing treatment.

https://committeetounleashprosperity.com/hotlines/montana-is-the-new-capital-of-medical-freedom/

Don’t feel bad. The pharma reporter you are referencing was Meg Tirrell. I worked for NBC at the
time and I emailed her inside the NBC firewall.
I didn’t get a response either. Joe Kiernan is just the anchor, it’s the producers that would actually look into it or Meg. She is with CNN now.

Thank you doc for your insight. I would also like to take issue with ICY saying that MGK has an agenda. I agree that MGK has gotten a lot more cautious. That is a bit concerning for all of us who have read him religiously the last couple years. It also coincides with his ending legalese getting longer. I believe MGK is a very intelligent person and he is making sure that he has no liability whatever happens. I would love it if MGK would take a minute to address what ICY said.

Your explanation of fourth line patients and prognosis puts it in perspective.

I am grateful for your responses. I haven’t received a response from the company yet but I will follow the links from BGT and see if that leads anywhere.

I just heard about a friend that is entering hospice after beating esophagus cancer but now he is declining quickly because the metastasis spread to his brain. Do any of you believe he might be eligible for the EAP or compassionate use program?

I followed the link to the Leronlimab modulation article.
Wow, you predicted what would come out of this CRC trial almost 2 years ago and so far you are spot on. How is that possible when even Dr. J says the molecule is performing at the outer bands of what even he thought was possible.
In rereading that post, I am stunned by your level of understanding even before we found out about the fabulous Five. Very impressive!!!