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| Cas No.: | 22862-76-6 |
| Chemical Name: | Anisomycin |
| Synonyms: | 3,4-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 |
| SMILES: | O(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] |
| Formula: | C14H19NO4 |
| M.Wt: | 265.305 |
| Sotrage: | 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO |
| Description: | Anisomycin is a potent protein synthesis inhibitor which interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system. |
| 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]. |
| 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]. |
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COA
| LOT NO. | DOWNLOAD |
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| 2018-0101 |
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| 2018-0101 |
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