DescriptionCurator's Comment: description was created based on several sources, including
http://www.ncbi.nlm.nih.gov/pubmed/3053566
http://www.piluli.kharkov.ua/drugs/drug/spiramitsin/
Curator's Comment: description was created based on several sources, including
http://www.ncbi.nlm.nih.gov/pubmed/3053566
http://www.piluli.kharkov.ua/drugs/drug/spiramitsin/
Spiramycin, a macrolide antibiotic, has been studied in the United States for the treatment of cryptosporidial diarrhea. Some reports suggest that spiramycin is useful in improving the symptoms of cryptosporidial diarrhea in some patients. It has been used in Europe and Canada for over 20 years to treat bacterial infections. Serious adverse effects from spiramycin are apparently rare, and no drug-associated deaths have been reported. Spiramycin inhibits translocation by binding to bacterial 50S ribosomal subunits with an apparent 1:1 stoichiometry. This antibiotic is a potent inhibitor of the binding to the ribosome of both donor and acceptor substrates. Spiramycin induces rapid breakdown of polyribosomes, an effect which has formerly been interpreted as occurring by normal ribosomal run-off followed by an antibiotic-induced block at or shortly after initiation of a new peptide. However, there is now convincing evidence that spiramycin, and probably all macrolides, act primarily by stimulating the dissociation of peptidyl-tRNA from ribosomes during translocation
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
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Target ID: CHEMBL2363135 Sources: http://www.ncbi.nlm.nih.gov/pubmed/3053566 |
Conditions
Condition | Modality | Targets | Highest Phase | Product |
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Curative | Rovamycine Approved UseUnknown |
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Curative | Unknown Approved UseUnknown |
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Curative | Unknown Approved UseUnknown |
Sample Use Guides
In Vivo Use Guide
Sources: http://www.piluli.kharkov.ua/drugs/drug/spiramitsin/
bacterial infections: 3 tablets/day; 5 days
toxoplasmosis: 1 g orally every 8 hours
Route of Administration:
Oral
In Vitro Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/27398599
Spiramycin significantly inhibited preadipocyte differentiation by attenuating intracellular lipid accumulation. Spiramycin also reduced the expression of adipogenic master regulators (PPARγ, C/EBPα, and SREBP1c) and their downstream target genes (FAS, aP2, and GLUT4) in 3T3-L1 cells. In addition, AMPK phosphorylation was increased by spiramycin treatment in 3T3-L1 cells during early differentiation
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Mixture
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