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The rifamycins specifically inhibit DNA-dependent RNA polymerase (nucleosidetriphosphate: RNA nucleotidyl transferase, DNA-dependent. E.C.2.7.7.6) of bacterial but not of mammalian origin.1' 2 Mizuno et al.3' 4 have shown that streptovaricin, a substance chemically related to the rifamycins, also specifically inhibits DNA-dependent RNA polymerase from E. coli but not from Ehrlich ascites cells. These authors demonstrated that DNA, CTP, Mg++, or Mn++, do not interact with the antibiotic. We have previously reported (a) that inhibition by the rifamycins is dependent on the amount of enzyme present,2 (b) that the sensitivity of bacterial and mammalian cells is strikingly different,2 and (c) that RNA polymerase isolated from bacteria resistant to rifamycin is not affected by the antibiotic.' All these findings suggest the occurrence of a direct interaction between enzyme and antibiotic.Using a 14C-labeled rifamycin derivative, we have now obtained evidence that RNA polymerase forms a very stable complex with the antibiotic with simultaneous loss of activity. Moreover, RNA polymerase from rifamycin-resistant mutants of E. coli does not form a complex with the antibiotic and is not inhibited.Materials and Methods.-CTP-'H was purchased from Schwarz BioResearch (Orange-

The effect of quindoxin on the synthesis of deoxyribonucleic acid (DNA), ribonucleic acid, and protein in Escherichia coli KL 399 was examined under aerobic and anaerobic conditions. In the absence of oxygen the synthesis of DNA was completely inhibited by 10 ppm of quindoxin, whereas the syntheses of ribonucleic acid and protein were not affected. Quinoxalin-di-N-oxides (QdNO) induce degradation of DNA in both proliferating and non-proliferating cells.polA, recA, recB, recC, exrA, and uvrA mutants were more susceptible than the corresponding repair-proficient strains. All strains were more resistant in the presence of oxygen. The potent in vivo activity of various quinoxaline-1,4-di-N-oxides (QdNO) against diverse bacteria, Entamoeba histolytica, and Chlamydiae of the psittacosis-lymphogranuloma venereum group has been known for more than two decades (9,24,29,35,50). Like many antibiotics (e.g., penicillin or tetracyclines) and chemotherapeutics (e.g., nitrofuran or sulfonamide), QdNO increase the live weight gain in young chickens, pigs, and calves when added to the diet (5,12,16,37). At present two QdNO, carbadox and olaquindox, are on the market as growth promoters in various countries; a third, quindoxin, has been withdrawn.QdNO were first prepared as potential antagonists of vitamin K activity, but such antagonism has never been demonstrated (24,35). Only a few further reports on the mode of action have been published. Studies on the effect of 2,3-dihydroximethyl-quinoxaline-1,4-di-N-oxide on the incorporation of radioactive precursors into deoxyribonucleic acid (DNA), ribonucleic acid (RNA), and protein in Escherichia coli revealed a specific inhibition of DNA synthesis (15). Morphological changes in cells of E. coli and Staphylococcus aureus treated with 2,3-dihydroxit Present address:

From a strain of Aspergillus nidulans var. echinulatus, A 32204, echinocandin, a novel polypeptide antibiotic complex with high and specific anti‐yeast activity was isolated. The main component, echinocandin B, was separated by counter‐current distribution. A tentative molecular formula C52H81N7O18 is discussed. The antibiotic is characterized by its IR. and NMR. spectra and by its characteristic hydrolytic degradation products: linoilic acid, L‐4‐hydroxyproline, L‐4‐oxoproline, (2S, 3S, 4S)‐4‐methyl‐3‐hydroxy‐proline, L‐threonine (2 mols), and 1‐(p‐hydroxyphenyl)‐3‐amino‐propan‐2‐one.