Curious why this is not toxic for the mitochondria of real cells if it is so bad for the cancer cells?
Is it because the therapy only blocks genesis of new mitochondria,and most people would have sufficient existing mitochondria to stay healthy through the course of the therapy?
The mitochondria in many cancer cell behave abberantly. For example, in many cases, they can start promoting glycolysis, in process known as the Warburg effect. They're also involved in other processes such as apoptosis and cell migration. I'd hypothesize that these drugs target pathways or processes that are dysregulated in the mitochondria of those cancers.
There better not be any comments on this thread about this paper from 2019 that didn't really make a huge splash and is entirely in cell culture that go "oh boy another cancer cure too bad they make it to the clinic." This is pretty much about as far from highly reliable and translation ready as you can get.
This is amazing and I do not mean to nit-pick but does this statement logically cohere?
>Also, the concentrations of antibiotics used here represent sub-antimicrobial levels of Doxycycline and Azithromycin, thereby avoiding the potential problems associated with antibiotic resistance.
Yes. The concentrations of the antibiotics are too low to select for resistance, because they do not significantly affect bacterial growth. (Without selection, no resistance).
μM is a measure of concentration, while μg is a measure of mass. If you meant "μg/L" (or some other measure of volume), it is conventional to use molarity when discussing drugs in basic as well as clinical (PK, PD) contexts.
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