Brilacidin's mechanism is three pronged unlike Remdesivir.
As Farrell and KMBJN succintly discussed at length here recently, the mechanism by which Brilacidin disrupts the viral membrane is unique and is extra-cellular, whereas Remdesivir is intra-cellular which itself presents a problem. Moreover, Brilacidin is anti-inflammatory and anti-bacterial, something that Remdesivir lacks.
A high SI of Remdesivir did enable it to succeed in-vivo and receive an EUA (though the extent of its success is under debate). Isn't there a higher probability for Brilacidin to succeed?
Note: I am not in the bio-medical field, so I used layman's terms to express my understanding. But the gentlemen I referred to above have explained it beautifully elsewhere.