How the target pathway of an anticancer drug alters after the cojugation of the drug with a nanoparticle? Is it just due to more specificity or what are the other reasons?
Hi Sudip. The answer is quite long and complicated and nevertheless not too exhaustive.
In short, the mechanism of action of the drug itself doesn't change. At best, in case the drug you are considering has more than one mechanism of action, you may redirect your formulation and favour one instead of the other.
However, what you ask in the title is not what you ask in the main message, and for that we need to be a bit more verbose. One of the challenge in drug delivery is having the maximum dose and the minimum side effects, which corresponds to the famous "magic bullet". In the design of drug delivery systems, for this reason, you try to use passive and active targeting strategies which should lead to a high concentration of the drug in the tissue/district of interest and lower (hopefully sub-effective) concentrations everywhere else. So, the drug itself does not become more potent BUT the therapeutic index is higher.
Then, again, you may want to consider what happens inside a single cell, and here the story gets out of control. One of the greatest problems we are still facing is the "effective" delivery. In other words, having a drug inside a cell doesn't mean the the drug will work. And I would use the word therapeutics here, rather than drug. You always have to hope, for example, to have endosomal escape and cytosolic release of the therapeutics. Or you have to circumvent the presence of transporters that can pump out your drug (or even your particles, sometimes) and in facts render the delivery absolutely ineffective. You may want to think of targeting specific organelles in the cells, like mitochondria. And once again, it is the combination of all these factors that render the drug "more potent".
hi. nonoparticle only affect on delivery and not related to mechanism of drug
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