RIFAMYCIN SV CAS 6998-60-3

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Model: MOS 6998-60-3
Place of Origin: Zhejiang,China (Mainland)
Name: RIFAMYCIN SV
CAS: 6998-60-3
Molecular Formula: C37H47NO12
Brand: MOSINTER
Content: 98%min
Molecular Weight: 697.77
Synonyms 1: Rifaximin EP Impurity C
Synonyms 2: 17,19,21-hexahydroxy-23-methoxy-2,4,12,16,18,20,22-heptamethyl-21-acetate
Category:

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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