Theralase Technologies Inc. V.TLT

The future (after NMIBC)

[DJDawg]

While all of us look forward to the ASCO data presentation as well as RDW's return (hopefully associated with more of an effort on the PR and JV fronts), I wanted to highlight how cool rutherrin is.

Recall that rutherrin is a combination of transferrin and TLD-1433. Transferrin usually binds iron and holds its hand to guide the iron to into cells via the transferrin receptor. The more transferrin receptors on a cell the more uptake of the rutherrin. Cancer cells are crazy avid for iron so they express extra transferrin receptors compared to regular cells.

Cancer therapy has always been challenged by the fact that you are trying to eradicate cells that, technically, are part of you, but have gone rogue, growing too fast, proliferating, jumping off into other locations. It is not like an antibiotic targetting a cell type that is not part of you. Bacteria are very different. Historically the way they they target cancer cells is with drugs that poison cells that are growing fast and hoping to poison more of the cancer cells than the patients' normal cells. This is why chemo causes hair to fall out and crazy gi upset. Because hair cells and gi tract cells are relatively more active in growth than, say, a single muscle cell or liver cell.

So the reason rutherrin is so cool is that it will preferentially go to any cells that love iron (such as cancer cells). Once there, a targetted beam of radiation, or light depending on setting can activate the killing mechanism of the molecule. I say light as you could see scenarios where surgeons remove most of the brain or lung cancer and then, having preloaded the patient with rutherrin, shine a specific light on the remaining operative field to kills off what they could not clean up compeletly. Or just do xray beams targetted to that area at a later date.

The big deal to me is the comparison of tranferrin receptors on normal cells to cancer cells. That is what translates into rutherrin uptake and killing effect.

See picture link below from source https://europepmc.org/article/MED/30034931

https://postimg.cc/PpRMSZH7

All the reddish brown is transferrin receptor expression. It looks like, no matter what the cancer, they love iron and love taking binding transferrin and recieving whatever transferrin is carrying. Transferrin bound to TLD-1433 is the classic trojan horse scenario.

Hope this is interesting. I'm no expert but love this science.

[Rumpl3StiltSkin]

Yep Dog, Nice synopsis. And, for whatever reasons, 1433/Rutherrin kicks off an immune response as well. Further protecting the patients from re-occurance.

[CancerSlayer]

  Agree..very nice overview of our ACT.  I would add that Rutherrin/TLD-1433 has been shown to perform well in more hypoxic environments compared to early generation photosensitizers (PSs), & Osmium (included in our IP) has proven to be even more promising in preclinical studies.  So you not only have the benefit of taking advantage of an increase in transferrin receptors