So the actinium-based radioligandary pure approach has the same principle as the beta-emitting. PSMA-targeted radioligandary pure approach will leverage the overexpression of the protein PSMA on the prostate cancer surface cells to bring a radioisotope, deliver energy, and kill these cells. But of course, it will also go to some other places in the body. PSMA is also expressed at normal levels in the salivary gland, in the kidney...
So the actinium-based radioligandary pure approach has the same principle as the beta-emitting. PSMA-targeted radioligandary pure approach will leverage the overexpression of the protein PSMA on the prostate cancer surface cells to bring a radioisotope, deliver energy, and kill these cells. But of course, it will also go to some other places in the body. PSMA is also expressed at normal levels in the salivary gland, in the kidney. And so that’s where the toxicity can come from. Because actinium delivers much more energy than lutetium, it creates also a higher toxicity profile in these organs at risk. And so the salivary gland toxicity, xerostomia, dry mouth, is more prominent with actinium-based agents rather than lutetium-based agents. So that was an issue so far. It’s good that we’re trying to define the right injected activity that can safely be used for the safe use of actinium-based PSMA-targeted agents. I think the long-term side effects will need to be monitored as well. On the kidney, for example, we know that there is a dose-response relationship that on long-term, maybe exposure to PSMA-targeted radioligand therapy approach can decrease the kidney function. So we have to investigate if it’s worse with actinium than with lutetium. And same thing with the bone marrow long-term toxicity, you know, myelodysplasia or other mechanisms that occur that impair the bone marrow function, we have to investigate if it’s worse with actinium than with lutetium. But for sure, on a short-term basis, what we know is that xerostomia is worse with actinium than with lutetium. So that’s one of the key differences. What medication methods do we have? Unfortunately, for salivary gland toxicity, there are not a lot of things that have been really validated. We try cooling of the salivary gland. Some people try injection of toxin botulin. You can do monosodium glutamate. You can do atropine. This molecule tends to decrease the level of uptake in this PSMA mechanism binding, but it does it in the tumor lesions and also in the normal organs. So, so far we haven’t found, unfortunately, a great way to mitigate the side effects except dosing schedule, playing with the time intervals and the injected activity.
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