Hi Mason, Are you even interested in having a productive...

Hi Mason,

Are you even interested in having a productive dialogue? Come to think of it, what is your objective here? You seem to love slinging mud at random intervals. Are you here as a knight in shining armour to save all IMU investors from losing money? For some reason, I doubt that's it; as it seems like you are hoping for IMU to fail regardless of which therapy it is. If that's the case, you inherently are hoping they fail at providing a more effective treatment for people with a terrible disease. I can't imagine why anyone would want that. Unless it somehow impacted them...So, is it as simple as others have mentioned that you wish IMU to fail to leave more space for RAC to succeed? Are you going to acknowledge your incorrect comments about immunized mice?

Ok, yes 'really' my comment was "Her-vaxx was tested initially in a patient population similar to the one where Herceptin was approved". What population was being trialled that led to Herceptin being approved? Gastric Cancer. What population was Her-VAxx being trialled within its Phase II...Gastric Cancer. Both of these factors went up against the standard of care. It wouldn't make much sense for Herceptin to be SOC and for IMU to test Her-VAxx in a population that had access to Herceptin, now does it?!

HER-Vaxx results for Gastric cancer:

The median OS for patients receiving HER-Vaxx plus chemotherapy was 13.9 (7.5, 14.3) months, compared to 8.3 (6.0, 9.6) months in patients treated with chemotherapy alone. Analysis showed a 42% survival benefit for patients treated with HER-Vaxx plus chemotherapy compared to chemotherapy alone. This translated into an OS HR of 0.580 (80% 2-sided CI: 0.362, 0.927) with a statistically significant p-value of 0.066.

Her-Vaxx adds NO toxicity for that OS benefit.
There was no difference in safety between the two treatment arms, indicating HER-Vaxx does not add toxicity to standard chemotherapy.

Herceptin results for Gastric cancer:
Median overall survival was 13·8 months (95% CI 12–16) in those assigned to trastuzumab plus chemotherapy compared with 11·1 months (10–13) in those assigned to chemotherapy alone (hazard ratio 0·74; 95% CI 0·60–0·91; p=0·0046).

Herceptin adds toxicity for that OS benefit.
The most common adverse events in both groups were nausea (trastuzumab plus chemotherapy, 197 [67%] vs chemotherapy alone, 184 [63%]), vomiting (147 [50%] vs 134 [46%]), and neutropenia (157 [53%] vs 165 [57%]). Rates of overall grade 3 or 4 adverse events (201 [68%] vs 198 [68%]) and cardiac adverse events (17 [6%] vs 18 [6%]) did not differ between groups.

Regarding your comments about other OVs' past performance, like with anything worth doing, it's worth doing it poorly first. I agree they haven't succeeded. Still, I and others are invested here, as we are leaning towards the likes of Yuman Fond and Saul Priceman, having learnt from past OV performance to assist them in developing CF33 + OnCARlytics. Actually, in the paper you referenced, Yuman Fong's studies are highlighted, quoting results of a previous therapy he had created (I assume the one he sold to Merck). So, there is already evidence of him leveraging past experience. Or is it your premise that all cancer research should stop if a method has failed in the past?! Regardless, as investors (and not scientists), we do put faith in YF, SP, and others getting the job done here. I, for one, am invested here, hoping for better cancer therapies and to achieve a significant return, and with that desire comes inherent risks. I nor many others are blindly expecting a win here, but the risk-to-return equation is still fantastic. And the 'research' you have shared thus far doesn't provide any objective evidence as to why CF33 won't work.

See below for data that shows a comparison of CF33 and T-Vec (I know there's a study out there that compares a few more, but I didn't have time to find it). The study in cancer cell lines showed that CF33 was two to three orders of magnitude more potent than the other two viruses. That is, a 100-fold to 1,000-fold lower dose of CF33 virus particles was required to kill tumour cells in culture, compared to the two other oncolytic viruses. However, as many IMU holders know, CF33 has a huge therapeutic window. So it's more potent at lower dosages AND has a larger runway to find its optimal efficacy. That bodes well for CF33, which is much better than T-Vec, perhaps even multiple times better.



Best selling = most revenue generated. After all, we are seeking commercial outcomes here.

Of course, cytotoxic agents you speak of have performed better than OVs since the word was invented. They also performed better than monoclonal antibodies before they were invented. Any and every human technical advancement had a worse track record than the incumbent, but that shouldn't stop progress. We differ in our definition of cytotoxic agents. I wouldn't call Keytruda a cytotoxic agent. Irrespective of that, you are comparing Keytruda and CF33 within your chosen context to make a point. What makes a therapy precision is targeting. Keytruda targets/blocks the PD-1 pathway. It generally works across different solid tumours, with the central assumption being that they express PD-1. CF33 has been designed for many types of solid tumours, distinct from other cytotoxic agents like chemo, which broadly targets fast replicating cells (whether they are cancerous or not), so thus lacking in precision. They are testing CF33 on all solid tumour types to test the theory that they have created an OV that kills many solid tumour types and leaves healthy cells alone. Solely solid tumours are the target. If they succeed in this, it will arguably be the most significant breakthrough in cancer treatment in decades.

Further to this, if they can achieve the abscopal effect and get solid tumours to express CD19, then regardless of whether CF33 can cause cancer cell death faster than cancer replication (or the patient's immune system attenuates CF33), the OnCARlytics/CAR-T factor will undoubtedly add significant efficacy not otherwise seen (based on CD19 efficacy) or tested in any other OV trail previously. I guess your take would be that "no one has used a CAR-T on solid tumours effectively" or "chemo has performed better than CAR-Ts since ???"

It's too early to be calling CF33 a success or failure for my mind. Still, I'm leaning towards success based on preclinical data and the issues around current OVs being alleviated with CF33. It is not a slam dunk yet, but it is hardly the lost cause you make it out to be.

Cheers.