Anisomycin

Anisomycin

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Anisomycin
Category Antineoplastic
Catalog number BBF-00692
CAS 22862-76-6
Molecular Weight 265.30
Molecular Formula C14H19NO4
Purity ≥98%

Ordering Information

Catalog Number Size Price Stock Quantity
BBF-00692 500 mg $239 In stock
BBF-00692 1 g $470 In stock

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Description

It is produced by the strain of Streptomyces griseolus. It inhibits protein synthesis. it has anti-fungal, anti-fine bacteria, anti-tumor and antigenic insect action.

Specification

Synonyms Flagecidin; NSC-76712; AI3-50846; NSC76712; AI350846; NSC 76712; AI3 50846
Shelf Life 2 years if stored properly
Storage 3 years -20℃powder;6 months-80℃in solvent
IUPAC Name [(2R,3S,4S)-4-hydroxy-2-[(4-methoxyphenyl)methyl]pyrrolidin-3-yl] acetate
Canonical SMILES O[C@@H]1[C@H]([C@@H](CC(C=C2)=CC=C2OC)NC1)OC(C)=O
InChI InChI=1S/C14H19NO4/c1-9(16)19-14-12(15-8-13(14)17)7-10-3-5-11(18-2)6-4-10/h3-6,12-15,17H,7-8H2,1-2H3/t12-,13+,14+/m1/s1
InChI Key YKJYKKNCCRKFSL-RDBSUJKOSA-N

Properties

Appearance Long White Acicular Crystal
Antibiotic Activity Spectrum neoplastics (Tumor); fungi; parasites
Boiling Point 398.7 °C at 760 mmHg
Melting Point 140-141 °C
Density 1.210 g/cm3
Solubility Soluble in Methanol, Ethanol

Reference Reading

1.microRNA let-7c is essential for the anisomycin-elicited apoptosis in Jurkat T cells by linking JNK1/2 to AP-1/STAT1/STAT3 signaling.
Zhou Z1,2, Lu X1, Wang J1, Xiao J1, Liu J3, Xing F1,2. Sci Rep. 2016 Apr 18;6:24434. doi: 10.1038/srep24434.
Anisomycin, an antibiotic produced by Streptomyces griseolus, strongly induces apoptosis in various tumor cells in vitro, superior dramatically to adriamycin. The present study aims to elucidate its detailed mechanistic process. The results showed that anisomycin sufficiently promoted the apoptosis in human leukemic Jurkat T cells at a quite low dose. microRNA let-7c (let-7c) contributed to the anisomycin-induced apoptosis, which could be abrogated by the inactivation of JNK signaling. The let-7c over-expression and the addition of its mimics facilitated the activation of AP-1, STAT1 and Bim by linking JNK1/2 to AP-1/STAT1, but rather inhibited the activation of STAT3 and Bcl-xL by connecting JNK1/2 to STAT3, followed by the augmented apoptosis in the cells. The let-7c deficiency reduced the AP-1, STAT1 and Bim activities, and enhanced the STAT3 and Bcl-xL, alleviating the anisomycin-induced apoptosis. The knockdown of the bim gene repressed the anisomycin-boosted apoptosis through the attenuation of the active Bak and Bax.

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Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2

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Tip: Chemical formula is case sensitive. C22H30N4O c22h30n40
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