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RIFAMYCIN SV CAS 6998-60-3 Rifaximin EP Impurity C
Rifamycin sodium salt
A class of antibiotics produced by the Mediterranean strand. There is a strong antibacterial effect on gram-positive coccus and tuberculosis bacillus, and the effect of staphylococcus aureus is strong, but the effect on gram-negative bacteria is weaker. No cross resistance was found with other class antibiotics or anti-tuberculosis medicine.
The rifamycins are a group of antibiotics that are synthesized either naturally by the bacterium Amycolatopsis rifamycinica or artificially. They are a subclass of the larger family ofansamycins. Rifamycins are particularly effective against mycobacteria, and are therefore used to treat tuberculosis, leprosy, and mycobacterium avium complex (MAC) infections.
The rifamycin group includes the "classic" rifamycin medicine as well as the rifamycin derivatives rifampicin (or rifampin), rifabutin, rifapentine, rifalazil and rifaximin.
Rifamycins have been used for the treatment of many diseases, the most important one being HIV-related tuberculosis. A systematic review of clinical trials on alternative regimens for prevention of active tuberculosis in HIV-negative individuals with latent TB found that a weekly, directly observed regimen of rifapentine with isoniazid for three months was as effective as a daily, self-administered regimen of isoniazid for nine months. But the rifapentine-isoniazid regimen had higher rates of treatment completion and lower rates of hepatotoxicity. However, the rate of treatment-limiting adverse events was higher in the rifapentine-isoniazid regimen.
The rifamycins have a unique mechanism of action, selectively inhibiting bacterial DNA-dependent RNA polymerase, and show no cross-resistance with other antibiotics in clinical use. However, despite their activity against bacteria resistant to other antibiotics, the rifamycins themselves suffer from a rather high frequency of resistance. Because of this Rifampin, and other rifamycins, are typically used in combination with other antibacterial medicine. This is routinely practiced in TB therapy and serves to prevent the formation of mutants that are resistant to any of the medicinemedicine
The antibacterial activity of rifamycins relies on the inhibition of bacterial DNA-dependent RNA synthesis.This is due to the high affinity of rifamycins for the prokaryotic RNA polymerase. The selectivity of the rifamycins depends on the fact that they have a very poor affinity for the analogous mammalian enzyme. Crystal structure data of the antibiotic bound to RNA polymerase indicates that rifamycin blocks synthesis by causing strong steric clashes with the growing oligonucleotide ("steric-occlusion" mechanism). If rifamycin binds the polymerase after the chain extension process has started, no inhibition is observed on the biosynthesis, consistent with a steric-occlusion mechanism. Single step high level resistance to the rifamycins occurs as the result of a single amino acid change in the bacterial DNA dependent RNA polymerase.
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