Why IMU is a multi multi bagger, page-24370

Yeah, I don't need to find another person to help me feel better about my analysis. If you're unhappy with my work and can't debunk it for yourself, find an oncologist who is prepared to put their reputation on the line to go against me publicly.

Here's why I don't need anyone speaking for me:

Over one year ago, I accurately predicted that CF33 failed to demonstrate efficacy through IV application in preclinical models and cautioned investors that this lack of efficacy would likely be reflected in human trials. The evidence to date supports this prediction, showing that single-agent IV CF33 and combination IV CF33/Keytruda resulted in zero responses.

22 April 2023: I'm wondering if anyone has addressed the fact that there is limited preclinical evidence that has demonstrated a significant benefit from intravenous administration of CF33 either as a single agent or in combination with an anti-PDL1 in every murine model tested?

27 April 2023: I believe the limited IV efficacy will be confirmed in humans, which will have significant clinical and commercial impact on the drug leading to a downstream effect on company shareholders.

28 April 2023: I would have a very different approach to this drug combination if there was a single shred of research that showcased that IV CF33/PDL1 significantly improved survival compared to CF33 and PDL1 as single agents (the fact that there are no single agent controls is another major issue of this preclinical trial).

Around April 2024 (two months ago), I made several predictions that have proven to be accurate. Firstly, there is now clear evidence that efficacy does not positively correlate with study duration (Figure 1). The GI patient population, excluding the CR outlier, included in the cholangiocarcinoma presentation clearly demonstrates progression after their 'best' response (Figure 1). Additionally, the available evidence indicates that dose is not correlated with efficacy, with the second dose tier being the only clinically relevant dose capable of driving a meaningful response in patients (Table 1).

I also correctly predicted that patients from dose-level 4 were unlikely to experience pseudoprogression; if they had responded, they would have been included in the Bell Porter presentation (Figure 2). Furthermore, I highlighted that the variance in intra-individual tumor responses and viral replication rates exposed CF33's inability to effectively address the heterogeneity of cancers, indicating a low likelihood of success for CF33 in the Phase 1 MAST trial. This is further evidenced by the Bell Porter presentation, which shows an update for only one patient while remaining silent about others (Figure 2). The overall response rate (ORR) for the P1 MAST trial is 7.5%, which is not indicative of a multi-billion-dollar platform drug – I challenge anyone to show me an example that contradicts this.

13 April 2024: It is impossible for you to come to the conclusion that increased study duration improves response to treatment based on the information available at this time. Therefore, what is actually happening is the opposite of what you are saying.

13 April 2024: In summary, the phase 1 trial data critically demonstrates that increased dosing of CF33 does not correlate with improved clinical outcomes in treating advanced solid cancers.

13 April 2024: It is impossible to say whether pseudoprogression is driving the increase in lesion size for cohort 4 without more data, but I believe the likelihood of pseudoprogression driving clinical responses in these patients to be extremely low.

13 April 2024: Despite some individual lesions showing complete reductions, the overall ineffectiveness across multiple lesions within the same patient underscores a significant challenge with intra-individual variability in cancer response. This variability, coupled with the lack of correlation between higher doses and enhanced viral replication, indicates that the optimal dosing regimen may not benefit from increased quantities of CF33.

13 April 2024: Based on the analysis above, I believe the likelihood of success from here is significantly low.

Figure 1: Every GI patient other than the CR progressed after achieving their 'best' response.

Table 1: Summarising dose levels and efficacy


The Bell Porter presentation demonstrating that there has been no further responses seen in patients.


The other things that I have said are yet to play out, but the available evidence is pretty damn convincing.

If you wonder why I don't care for another persons opinion, it's because I've been right almost 100% of the time with IMU. I wasn't telling you to buy at 40-60c like others, and I sleep like a baby at night knowing I tried to help a huge volume of people understand extremely complex science in a competitive industry.