This is due to the observation that 3 amino-acid analogues converted into AHBA in cell-free extracts of  A. mediterranei. The rif cluster is responsible for the biosynthesis of rifamycins. It contains genes rifG through rifN, which were shown to biosynthesize AHBA. [10]  RifK, rifL, rifM, and rifN are believed to act as transaminases in order to form the AHBA precursor kanosamine. "RifH" encodes aminoDAHP synthase that catalyzes the condensation between 1-deoxy-1-imino-d-erythrose 4-phosphate and phosphoenolpyruvate. RifA through rifE encode a type I polyketide synthase module, with the loading module being a non-ribosomal peptide synthetase. In all, rifA-E assemble a linear undecaketide and are followed by rifF, which encodes an amide synthase and causes the undecaketide to release and form a macrolactam structure. Moreover, the rif cluster contains various regulatory proteins and glycosylating genes that appear to be silent. Other types of genes seem to perform post-synthase modifications of the original polyketide. Derivatives
Lepetit introduced Rifampicin, an orally active rifamycin, around 1966. Rifabutin, a derivative of rifamycin S, was invented around 1975 and came onto the US market in 1993. Hoechst Marion Roussel (now part of Aventis) introduced rifapentine in 1999. Rifaximin is an oral rifamycin marketed in the US by Salix Pharmaceuticals that is poorly absorbed from the intestine. It has been used to treat hepatic encephalopathy and travelers diarrhea. Currently available rifamycins
Rifampicin or Rifampin
Rifabutin
Rifapentine
Rifaximin
Aemcolo

References
Bibliography
Sensi. et al., Farmaco Ed. Sci. (1959) 14, 146-147 - the paper announcing the discovery of the rifamycins. Thieman et al. Arch. Microbiol.
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