We are looking, quite hard, in fact. Mycobacterium tuberculosis is among the most studied microörganisms.
Like HIV, it is notable particularly for being able to defeat the attempts of the immune system cells to kill it, and it in fact infects and reproduces within macrophages. Medical researchers have done a lot to understand how this is possible and we (as in humanity) have identified several enzymes and related biomolecules which seem to be crucial to this process, which we might be able to inhibit with a targeted drug.
However, all of this scientific research has the usual problem that it is very difficult and expensive. In order to inhibit the enzyme, the drug must be absorbed by the body, and then make its way into the macrophages, and then it still must be active, and have no other toxicity to the host. It is easy to say "just inhibit isotuberculosinol synthase", but it is much harder to do.
As I understand it, this is also the reason why treating tuberculosis requires such long courses of antibiotics. When treating a normal infection, we are basically just killing most of the pathogens, and we hope that the immune system will mop up the rest. In the case of M. tuberculosis, the drugs have to kill all of the bacteria, which is why multidrug therapy is basically always used and the patient must continue treatment long after symptoms seem to have disappeared. Even when patients have recovered, they are always considered to be at risk of still having latent tuberculosis, which is why hospital screenings often feature a question like "have you ever had a positive test for tuberculosis?"
