Catalyzes the hydrolysis of fructose 1,6-bisphosphate to fructose 6-phosphate (PubMed:15470127, PubMed:21451980). Seems to be the major FBPase of M.tuberculosis and to play a key role in gluconeogenesis for conversion of lipid carbon into cell wall glycans. Does not display activity against inositol 1-phosphate (PubMed:15470127). beta-D-fructose 1,6-bisphosphate + H2O = beta-D-fructose 6-phosphate + phosphate Has an absolute requirement of bivalent metal ions Mg(2+) or Mn(2+). Is inhibited by Li(+) and by inorganic phosphate. kcat is 1.0 sec(-1). Optimum pH is 9.0. Is active over a pH range from 7 to 9. Retains its full activity until 30 degrees Celsius. A significant loss in the activity (65% loss) is noted at 40 degrees Celsius. Complete inactivation of the enzyme occurs at temperatures greater than 50 degrees Celsius. Carbohydrate biosynthesis; gluconeogenesis. Homooligomer (PubMed:21451980). Probably a dimer (PubMed:21636919). Is expressed during exponential growth, with mRNA levels approximately half of the level of sigA. Cells lacking this gene are shown to be highly attenuated in a mouse tuberculosis model (PubMed:14569030). However, another study shows that in a mouse model of M.tuberculosis infection, cells lacking this gene are able to replicate and persist in lungs similar to the wild-type strain (PubMed:26258286). The mutant cells grow on gluconeogenic carbon sources and have detectable FBPase activity, due to the alternative FBPase (Gpm2, Rv3214) (PubMed:26258286). A third study shows that disruption of glpX leads to a growth profile comparable to that of wild-type when grown on the standard enrichment media, but growth is dysgonic with individual gluconeogenic substrates such as oleic acid, glycerol and acetate, and the mutant strain fails to efficiently replicate during the acute phase (i.e. first 30 days post-infection) of infection and begins to die thereafter (PubMed:26397812). Cells lacking both glpX and gpm2 grow as well as wild-type on glucose, but are unable to grow on any of the gluconeogenic carbon sources tested (glycerol, acetate and butyrate); the growth defect on gluconeogenic carbon sources is fully complemented by restoring expression of either GlpX or Gpm2. This double mutant lacks detectable FBPase activity and accumulates FBP. It is also severely attenuated in a mouse model of infection, as it fails to replicate in mouse lungs during the first 10 days of infection and begins to die thereafter (PubMed:26258286). Gluconeogenesis is critical to M.tuberculosis ability to establish infection and is necessary for its survival in the host. Belongs to the FBPase class 2 family.