Yes, this is one reason why an approach using a form of soluble ACE2 is so promising; mutations that would normally cause e.g. monoclonal antibodies to stop working (as detailed with the mink mutation) would in theory not stop the 'decoy receptor' approach.

Despite the fact soluble ACE2 is not looking like it'll be developed in time to impact the pandemic, there is a silver lining:

If you look at the original paper (https://www.thelancet.com/journals/lanres/article/PIIS2213-2...), you'll note they include details on angiotensin peptide levels in the patient.

Interestingly, in this n=1 case report, it looks like the soluble ACE2 is unlikely to have worked as an antiviral; the patient already had a high level of antibodies, as you can see in the Lancet paper above. So /if/ the patient's improvements can be ascribed to the soluble ACE2 treatment, it's likely the improvement was because of the effect the soluble ACE2 had on the person's renin-angiotensin system.

And if this holds, then it's likely many of these same improvements would be possible using a common class of widely-available blood pressure medications called ARBs.

This approach would not neutralize the virus, but instead stop the body from damaging itself. That's the theory, at least.

There are ~20 trials of ARBs for COVID-19 in progress now, though almost all are underdosed.