Do drugs for Mycobacterium Tuberculosis cofactor F420 prevent the evolution of resistance

Tuberculosis (TB) is an infectious disease that affects the majority of the world. The current treatment TB involves a combination of 5 to 6 antibiotics due to the development of resistance to many of these drugs in Mycobacterium tuberculosis (Mtb). These drugs usually consist of first-line drugs like isoniazid and rifampicin and second-line drugs like fluoroquinolones. Hence, drugs that currently exist to combat Tuberculosis only work when combined with other antibiotics, since extensively-drug resistant tuberculosis (XDR TB) has rendered them less effective against Mycobacterium Tuberculosis(Mtb).
In this paper, I have investigated how different drugs that exist could inhibit cofactor F420 in the metabolism of Mtb. These include Tamiflu, AZD6482, Arfomoteral, and Minocycline. The binding affinity of these drugs, which are similar in structure to cofactor F420, was found against different F420-containing proteins in Mtb, and hence their possible use in the future was investigated. Hence, hypothetically if such drugs are able to bind to cofactor F420-containing enzymes, they can inhibit them. This could give rise to the theory of allowing mtb to undergo antibiotic stress, since F420 has been found to be crucial in pathways that combat this stress. Therefore, mtb would undergo stress, decreasing its chances of survival and subsequently decreasing the possibility of cells surviving and mutating. However, this is an indirect relation and needs further experimental investigation.