Anisomycin chemical structure
Chemical structureResearch use only
CAT. NO. DC22604Featured

Anisomycin

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Product overview

Description & Application

Anisomycin is a potent protein synthesis inhibitor which interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system.

ParameterValue
Chemical NameAnisomycin
CAS No.22862-76-6
Synonyms3,4-Pyrrolidinediol,2-[(4-methoxyphenyl)methyl]-, 3-acetate, (2R,3S,4S)-;Anisomycin;Anisomycin from Streptomyces griseolus;Anisomycin,(2R,3S,4S)-2-[(4-Methoxyphenyl)methyl]-3,4-pyrrolidinediol3-acetate;(2R,3S,4S)-2-(4-Methoxybenzyl)-3,4-pyrrolidinediol 3-Acetate;2-p-methoxyphenylmethyl-3-acetoxy-4-hydroxypyrrolidine;ANISOMYCIN,STREPTOMYCES GRISEOLUS;antibioticpa-106;Wuningmeisu C;Flagecidin;(-)-Anisomycin;(2R,3S,4S)-2-(p-Methoxyphenylmethyl)-3-acetoxy-4-hydroxypyrrolidine;NSC 76712;(2R,3S,4S)-4-hydroxy-2-(4-methoxybenzyl)pyrrolidin-3-yl acetate;NSC76712;(2R,3S,4S)-2-(p-Methoxybenzyl)-3,4-pyrrolidinediol 3-acetate;Upjohn 204t3;2-(p-Methoxybenzyl)-3,4-pyrrolidinediol 3-acetate;6C74YM2NGI;MLS001066392;Anisomycin, Streptomyces griseolus;1,4,5-Trideoxy-1,4-imino-5-(p-methoxyphenyl)-D-xylo-pentitol 3-acetate;SMR00047
FormulaC14H19NO4
M.Wt265.305
SMILESO(C(C([H])([H])[H])=O)[C@]1([H])[C@]([H])(C([H])([H])N([H])[C@]1([H])C([H])([H])C1C([H])=C([H])C(=C([H])C=1[H])OC([H])([H])[H])O[H]
Purity>98%
Storage2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO

Biological Activity

Anisomycin is a potent protein synthesis inhibitor which interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system.

In Vitro

To examine whether JNK has a core role in colistin-induced neurotoxicity in PC-12 cells, an SP600125 (a highly selective inhibitor of JNK) and Anisomycin (a potent activator) are used in this study. In order to select an appropriate concentration, PC-12 cells are treated with a range of SP600125 (0-80 μM) and Anisomycin (0-20 μM) respectively for 24 h. The results show that the cells viability significantly decreases by SP600125 treatment in a concentration-dependent manner, observed at the concentrations greater than 20 μM (p<0.01). Similarly the cells viability is inhibited by Anisomycin treatment (≥8 μM) (p<0.05) [1].

In Vivo

Disruption of TNFRp55/p75 attenuates Anisomycin-induced ventricular functional improvements. Anisomycin results in an improvement in left ventricular developed pressure (LVDP), which disappears in animals with disruption of TNFR p55/p75. In addition, the Anisomycin-induced improvement in LVEDP in wild-type animals is eliminated by deletion of TNFR p55/p75. Likewise, disruption of TNFR p55/p75 abrogates the recovery of rate pressure product (RPP) elicited by pretreatment of Anisomycin. TNFR p55/p75-/- mice without Anisomycin treatment do not show differences in cardiac functional recovery compared with the control wild-type mice. There are no significant differences in heart rate between wild-type and TNFR p55/p75-deficient mice. To see whether Nox2 is involved in Anisomycin-induced myocardial protection, Nox2-deficient mice are treated with Anisomycin. The improvement in the LVEDP in Anisomycin-treated mice is eliminated in Nox2-/- mice compared with wild-type mice. In addition, recovery of RPP in wild-type mice treated with Anisomycin is mitigated in Nox2-/- mice. Nox2-/- mice without Anisomycin treatment do not show the difference in cardiac functional recovery compared with wild-type control mice[2].

References & source

DC Chemicals original product information

Published experimental findings depend on the model and assay conditions. They do not guarantee equivalent performance in every application. For laboratory research use only.

Product documentation

Refer to the certificate supplied with your lot for batch-specific release results.

Handling guide

2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO

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