Charting Only, page-118

Interesting reference to TransMolecular's 131-I TM-601. Whilst these therapies may appear similar given they both utilise Chlorotoxin's Glioblastoma binding ability. However, the difference is the "payload". In CHM's case, it's a CAR-T cell immunotherapy.

As Carl June said:
"[...] So it's been about 20 years just making the platform of how to make the T cells be reprogrammed, so that they could then be this CAR T cell. And now it's actually not so difficult because it is only one part that needs to be swapped out. It's just like changing the program a little bit and then now they could be NET specific rather than leukaemic specific T cells. [...]"

https://hotcopper.com.au/threads/ann-licenses-viral-vector-technology-from-penn-for-cdh17.6816082/page-18

In our case, CLTX-EQ-28ζ CAR T cells.

There is a lot of information available in the paper published here:
Chlorotoxin-directed CAR T cells for specific and effective targeting of glioblastoma

It also mentions TransMolecular's early approaches.

A few things I found particularly interesting here:

"Of note, CLTX-EQ-28ζ CAR T cells were effective against PBT-TS lines from four different patients that displayed distinct IL13Rα2, HER2 and EGFR expression profiles. In particular, while IL13Rα2-targeted CAR T cells failed to respond to the PBT-TS lines with low-to-negative IL13Rα2 expression (PBT003-4-TS, PBT138-TS), CLTX-EQ-28ζ CAR T cells recognized and responded to all four TS lines (Fig. 2, ,BB--D).D)."

That is a big statement, given that "One of the major obstacles limiting CAR T cell therapeutic efficacy has been tumor heterogeneity, which is particularly substantial in GBMs. The classification of GBM subtypes has illustrated the heterogeneity across patients, and more recent studies using single cell sequencing also revealed considerable genetic variations among intratumoral subpopulations, as well as plasticity between different cellular states (12, 13). Efforts to develop CAR T cell immunotherapy must contend with this high diversity of potential target antigen expression. For example, CAR T cells targeting IL13 receptor α2 (IL13Rα2) are under active clinical development (7, 14), as we and others have reported that expression of IL13Rα2 is frequently found on GBM tumors, and on a high proportion of cells within these tumors (15). However, after treating patients with IL13Rα2-targeted CAR T cells, instances of tumor recurrence with loss and/or reduced expression of IL13Rα2 has been observed (7, 14). Similar results have been reported following EGFR variant III (EGFRvIII)-targeted immunotherapies, with lower EGFRvIII expressions in recurrent tumors post-therapy (9, 16). In general, tumors are able to rapidly adapt to the selection pressures imposed by immunotherapies, resulting in relapsed tumors with distinct intratumoral cellular profiles (17), so-called antigen escape."

"Tumor recurrence remains a barrier to successful immunotherapy for GBM. Recurrence is commonly associated with the presence of cell subpopulation(s) resistant to radiotherapy and chemotherapy, and characterized by high tumor-initiating potential, GSCs (37). The virulence of GSCs has made them a critical consideration of GBM-targeted immunotherapy (59), and previous studies have demonstrated that GSCs can be as responsive to CAR T cell-mediated cytotoxicity as more differentiated GBM cells (33, 38, 39), despite their intrinsic immunosuppressive properties (60). Functional evaluations of CLTX-CAR T cells throughout this study have utilized patient-derived TS lines, which maintain stem cell-like properties under appropriate culture conditions (34). Further, since the identification of GSCs using single surface markers may confer bias towards certain GBM molecular subtypes (61), we used two different markers, CD133 and CD44, to identify GSC-like subsets in primary tumor samples, and showed that CLTX-Cy5.5 binding was similar in both GSC subsets and in non-GSC populations. Our results indicate that CLTX-CAR T cells inherit the binding properties of CLTX peptide, and thus will be active against both GSC and non-GSC populations in patient tumors, suggesting the potential to target the “seeds” of GBM recurrence."

I couldn't justify making an investment decision based on a conclusion drawn on the possible effects of a therapy in a compex indication such as Glioblastoma, solely based on the vehicle used to deliver (different) "payloads". Or maybe I am simply biased because I have done the complete opposite, accumulating over the past few months haha