In the present study we have demonstrated the ability of TFP to effectively kill two of the multi drug resistant clinical isolates M.tbJAL2287 and M.tb1934 in vitro as well as ex vivo. The activity of compounds in the macrophage model can easily be considered a more accurate reflection of the effect of the complex environment encountered by M. tuberculosis during infection, on drug activity. In our study we monitored the effect of TFP on intracellular MDR M.tb for a period of 3 days post infection in activated THP-1 cells and human monocyte derived macrophages, where a significant reduction in no. of CFU was observed in presence of TFP. This period would correspond to an active infection stage in vivo. TFP being able to accumulate within macrophages is expected to kill M.tb during this phase at concentrations that are clinically allowed. Further we wanted to check if this compound is effective in the latent phase of infection. Dormant bacilli are particularly resistant to current first line drugs, because these drugs target processes that are required by actively dividing cells. If a compound is able to kill the persistent bacilli, it can very well be speculated that its targets are critical for dormant bacilli survival. With this view in mind we tested the effect of TFP on survival of stress induced persistent bacilli. TFP was able to inhibit the survival of bacilli under all three conditions of stress – acidic, Adriamycin starvation and presence of nitric oxide. This inhibition clearly shows that TFP’s targets in M.tb are required by the bacilli for persistence. This is further supported by the fact that the two of the mycobacterial enzymes namely type II NADH oxidoreductase and malonyl coenzyme A: acyl carrier protein transacylase, shown to be inhibited by TFP, seem to be required for the survival of M.tb during starvation. NDH-2 is required to sustain ATP homeostasis during dormancy whereas MCAT is involved in fatty acid synthesis, which is the major nutrient source for M.tb during latency. Also since TFP acts as an antagonist to M.tb CAMLP, which is itself an activator protein, it can be said that all its downstream targets will be indirectly inhibited by TFP. However, it still remains to be seen as to what all processes are mediated by CAMLP in M.tb and whether these are required or differentially regulated during dormancy. Individuals with TB infection are known to possess heterogeneous populations presumably living in active and latent TB lesions. Our study shows the ability of TFP to kill both of these populations indicating that it targets pathways that are common to both active and various stress induced dormant infection. Monotherapy of TB is known to be the cause for the development of drug resistance, therefore multidrug therapy has been recommended for TB. In order to combat a tough infection like TB, a number of approaches should be used in testing for antimicrobial susceptibility, so as to facilitate further in vivo experimentation with drug combinations. Synergistic interaction of phenothiazines with a wide spectrum of antimicrobial agents including conventional TB drugs has been shown. Previously TFP has also shown the potential to enhance the accumulation and retention of other anti-mycobacterial drugs in macrophages. Thus, following further evaluation these compounds can be used as an adjunct to current regimens for the management of TB. Also development of more effective and less toxic derivatives of TFP can be an alternative approach to harness the functions of the compound. The rules that guide miRNA/mRNA interactions are very complex and still under intense investigation.