IMU (ASX) From the Professor...

Originally posted by Mason14: ↑

This is the height of misleading pseudoscience biased garbage.

Can someone from the group of 34 post the professors analysis on the HER-vaxx data? If possible, separate p1b and p2, as they are similar but have unique weaknesses. If the professor was great, he would have seen what I and IMU management saw.

The single cholangiocarcinoma patient is not the mean, it's the outlier. The average of the data set so far points to ineffectiveness and I am not confident that increasing the dose is going to produce more effect.

Pexa-Vec is an OV therapy within the same poxviridae family as CF33. Let's play a game - here are the results from a P1 trial of Pexa-vec in liver cancer to find the optimal p2 dose in comparison to IMUs CF33 data to date.

Can you guess which compound is 1 and 2? More than 85% of the time, both drugs fail to achieve a meaningful response. The clear weakness of the P1 Pexa-vec data follows through to eventually proving that single agent Sorafenib outperforms combination Pexa+sorafenib in a P3 trial. What does that say about the future of CF33 and the three clinical programs? Risk.

Pexa-vec is from the same family of virus as CF33, though it is impossible to state whether dose ranges would be the same for each. In any case, a 10^9 appears to be the ceiling for Pexa. That data has not been released by IMU yet, so we will wait and see.

A lot of you are oblivious or maybe moreso ignorant to how much data is out there that is against the success of CF33 and OV therapy in general. I'm hoping that an increase in dose improves efficacy significantly and that there are no DLTs.

Compound 1: CF33
Compound 2: Pexa-vec

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Can someone please send this to the pretender?

More data on the GI-cancer patients from prior cohorts.

IMU: "The objective response rate was 14% while the disease control rate was 86% (Figure 3)."

Proof that “best response” is a terrible measure of clinical efficacy. Within 100-days of treatment initiation, 86% of patients' target lesions had already increased or began increasing in size - ie. they started progressing. Patients would have received 3 doses by day 35 and 6 doses of CF33 by day 100 (Q3W with 2 doses C1D1 and C1D8). This highlights lack of clinical efficacy and adaptive resistance to treatment in this patient population.

IMU: “A second patient with cholangiocarcinoma who previously progressed on checkpoint blockade therapy achieved stable disease for >5 months upon receiving IV-administered CF33-hNIS (3.0x10^7 PFU).”

They are referencing patient US03-008 who experienced the greatest increase in tumor size relative to other patients (circled in red in Figure B). The average tumor size began increasing after the first review. This highlights lack of clinical efficacy and adaptive resistance to treatment in this patient.

Below is a table summarising each patient's tumor type, best response, dose, administration route, and final change in lesion size as a percent. Clearly, the CR is not the mean. IV monotherapy appears to be completely useless in this patient population and dosing regimens.

Still waiting for meaningful clinical data. Small chance of success for rare cancer indication expansion within a very small oncolytic viral therapy market, which multiple sources state it is significantly below current MC. I suspect a realistic price target for a meaningful gain is 1.5c to 2c.