1. Immunology/Inflammation
  2. Toll-like Receptor (TLR)

Atractylenolide I 

Cat. No.: HY-N0201 Purity: 99.08%
Handling Instructions

Atractylenolide I is a natural compound extracted from largehead atractylodes rhizome; induce apoptosis and bring about cytotoxicity of human promyeloleukemic HL-60 cells; TLR4-antagonizing agent.

For research use only. We do not sell to patients.

Atractylenolide I Chemical Structure

Atractylenolide I Chemical Structure

CAS No. : 73069-13-3

Size Price Stock Quantity
10 mM * 1 mL in DMSO USD 99 In-stock
Stock in the United States
Estimated Time of Arrival: December 31
5 mg USD 90 In-stock
Stock in Sweden
Estimated Time of Arrival: December 31
10 mg USD 150 In-stock
Stock in Sweden
Estimated Time of Arrival: December 31
50 mg USD 490 In-stock
Stock in Sweden
Estimated Time of Arrival: December 31
100 mg   Get quote  
200 mg   Get quote  

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  • Biological Activity

  • Protocol

  • Technical Information

  • Purity & Documentation

  • References

Description

Atractylenolide I is a natural compound extracted from largehead atractylodes rhizome; induce apoptosis and bring about cytotoxicity of human promyeloleukemic HL-60 cells; TLR4-antagonizing agent. IC50 value: Target: TLR4 antagonist in vitro: The ID(50) values of atractylenolide I were 15.15 mg/kg and 3.89 microg/ml for inhibiting the vascular index in vivo and microvessel outgrowth in vitro, respectively. Atractylenolide I could dose-dependently inhibit the production of nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF) activity in the flute of mouse air pouch and the peritoneal macrophages stimulated by lipopolysaccharide (LPS) [1]. ATL-I showed no inhibitory effect on cell viability at concentrations ranging from 1 μM to 100 μM and markedly reduced the release of IL-6 and TNF-α at a concentrate-dependent manner. In addition, ATL-I suppressed the activity of nuclear NF-κB and the phosphorylation of ERK1/2 and p38 in LPS-treated RAW264.7 cells [2]. AT-I inhibited the self-renewal capacity of gastric stem-like cells (GCSLCs) by suppression of their sphere formation capacity and cell viability. AT-I attenuated gastric cancer stem cell (GCSC) traits partly through inactivating Notch1, leading to reducing the expressions of its downstream target Hes1, Hey1 and CD44 in vitro [3]. AO-I was found to attenuate paclitaxel-induced protein expression of IL-6, VEGF and survivin, and to enhance early apoptosis and growth inhibition in MyD88(+) EOC cells; AO-I was shown to fit into the hydrophobic pocket of human MD-2 and to partially overlap with the binding site of paclitaxel by docking simulations, suggesting that AO-I may block the MD-2-mediated TLR4/MyD88-dependent paclitaxel signaling in MyD88(+) EOC cells [4]. in vivo: In the in vivo study, ATL-I effectively suppressed tumor growth (A549) in transplanted tumor nude mice with up-regulation of caspase-3, caspase-9, and Bax and down-regulation of Bcl-2 and Bcl-XL [5].

References
Molecular Weight

230.3

Formula

C₁₅H₁₈O₂

CAS No.

73069-13-3

SMILES

O=C1C(C)=C(C[[email protected]@]23[H])C(O1)=C[[email protected]@]3(C)CCCC2=C

Storage
Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month
Shipping

Room temperature in continental US; may vary elsewhere

Solvent & Solubility

10 mM in DMSO

* "<1 mg/mL" means slightly soluble or insoluble. "≥" means soluble, but saturation unknown.

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Atractylenolide I
Cat. No.:
HY-N0201
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