I didn't click, but there is a paper that showed that, for in vitro cultured cells, IVM at high concentration can block viral entry to some extent by targeting the S-Ace2 receptor interaction, much as it has been shown to disrupt cell entry for other viruses. that is the "same mechanism" you are talking about. The problem, from a physiological standpoint, is delivering the drug at an efficacious concentration to the necessary site of action, which in this case is the external surface of epithelial cells lining your respiratory track, requires a very high circulating concentration. Since IVM is metabolized and cleared rapidly, there are studies showing that it may not be possible to sustain the necessary circulating concentration for a pharmacologically relevant period of time. As has been discussed here, at high concentrations IVM can also cross the blood brain barrier and enter the central nervous system, at which site it is a rather potent neurotoxin because it can target the receptors involved in neuronal signalling. So there is a drug targeting problem with IVM for respiratory viruses. Snorting IVM might be one possibility; I imagine somebody is trying it.
Rather than preventing infection, it's possible that IVM may be of value at high concentration at limiting infections once they become more systemic, or once the permeability of the aveolar epithelium becomes altered due to immune cell infiltration as a Cov-2 infection really gets going. Because IVM can disrupt so many types of small molecule/receptor interactions, it is also a good anti-inflmmatory, and it's clear at this point that IVM can work like some of the other anti-inflammatories that are being used to treat COVID.
For the rest of it, going from "Ivermectin may very well be less efficient at the doses safe for human consumption" to the all rest of it, others can play with it if they think it has any relevance.