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The biological activity of rifamycins relies on the inhibitionof DNA-dependent RNA synthesis . Thisis due to the high affinity of rifamycins to prokaryotic RNApolymerase. Crystal structure data of the antibiotic bound to RNApolymerase indicates that rifamycin blocks synthesis by causingstrong steric clashes with the growing oligonucleotide. Ifrifamycin binds the polymerase after the chain elongation processhas started, no effect is observed on the biosynthesis, which isconsistent with a model that suggests rifamycin physically blockschain elongation . Inaddition, rifamycins showed potency towards HIV. This is due totheir inhibition of the enzyme reverse transcriptase, which isessential for tumor persistence. However, rifamycin's potencyproved to be mild and this never lead to their introduction toclinical trials.

Protein Synthesis and Site of Action of Antimicrobials that Inhibit Protein Synthesis

The rifamycins are also the products of . Rifampicin is a semisynthetic derivative of rifamycin that is active against Gram-positive bacteria (including Mycobacterium tuberculosis) and some Gram-negative bacteria. Rifampicin acts quite specifically on eubacterial RNA polymerase and is inactive towards RNA polymerase from animal cells or towards DNA polymerase. The antibiotic binds to the beta subunit of the polymerase and apparently blocks the entry of the first nucleotide which is necessary to activate the polymerase, thereby blocking mRNA synthesis. It has been found to have greater bactericidal effect against M .tuberculosis than other anti-tuberculosis drugs, and it has largely replaced isoniazid as one of the front-line drugs used to treat the disease, especially when isoniazid resistance is indicated. It is effective orally and penetrates well into the cerebrospinal fluid and is therefore useful for treatment of tuberculosis meningitis and meningitis caused by Neisseria meningitidis.


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Rifampicin - WHO | World Health Organization

The cluster is responsible for the biosynthesis of rifamycins. It contains genes through , which were shown to biosynthesize AHBA.[10] , , , and are believed to act as s 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. through encode a type I polyketide synthase module, with the loading module being a . In all, assemble a linear undecaketide and are followed by , which encodes an amide synthase and causes the undecaketide to release and form a macrolactam structure. Moreover, the 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.


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Rifamycin, a group of tuberculosis-fighting antibiotics, achieves a similar effect by inhibiting the synthesis of RNA, a molecule involved in translating the body's DNA into proteins.

Treatment of Tuberculosis — NEJM

Chloramphenicol has a broad spectrum of activity but it exerts a bacteriostatic effect. It is effective against intracellular parasites such as the rickettsiae. Unfortunately, aplastic anemia, which is dose related develops in a small proportion (1/50,000) of patients. Chloramphenicol was originally discovered and purified from the fermentation of a , but currently it is produced entirely by chemical synthesis. Chloramphenicol inhibits the bacterial enzyme peptidyl transferase thereby preventing the growth of the polypeptide chain during protein synthesis.

Tuberculosis is often a difficult infection to treat

Chloramphenicol is entirely selective for 70S ribosomes and does not affect 80S ribosomes. Its unfortunate toxicity towards the small proportion of patients who receive it is in no way related to its effect on bacterial protein synthesis. However, since mitochondria probably originated from procaryotic cells and have 70S ribosomes, they are subject to inhibition by some of the protein synthesis inhibitors including chloroamphenicol. This likely explains the toxicity of chloramphenicol. The eukaryotic cells most likely to be inhibited by chloramphenicol are those undergoing rapid multiplication, thereby rapidly synthesizing mitochondria. Such cells include the blood forming cells of the bone marrow, the inhibition of which could present as aplastic anemia. Chloramphenicol was once a highly prescribed antibiotic and a number of deaths from anemia occurred before its use was curtailed. Now it is seldom used in human medicine except in life-threatening situations (e.g. typhoid fever).

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Effects on Nucleic Acids Some chemotherapeutic agents affect the synthesis of DNA or RNA, or can bind to DNA or RNA so that their messages cannot be read. Either case, of course, can block the growth of cells. The majority of these drugs are unselective, however, and affect animal cells and bacterial cells alike and therefore have no therapeutic application. Two nucleic acid synthesis inhibitors which have selective activity against procaryotes and some medical utility are nalidixic acid and rifamycins.