We Offer Worldwide Shipping
Login Wishlist

Alantolactone

$78

  • Brand : BIOFRON

  • Catalogue Number : BF-A3012

  • Specification : 95%

  • CAS number : 546-43-0

  • Formula : C15H20O2

  • Molecular Weight : 232.32

  • PUBCHEM ID : 72724

  • Volume : 20mg

In stock

Quantity
Checkout Bulk Order?

Catalogue Number

BF-A3012

Analysis Method

HPLC,NMR,MS

Specification

95%

Storage

-20℃

Molecular Weight

232.32

Appearance

White crystalline powder

Botanical Source

Dendrobium officinale,Atalantia buxifolia,Dicliptera chinensis,Inula helenium,Inula japonica

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1CCCC2(C1=CC3C(C2)OC(=O)C3=C)C

Synonyms

8b-Hydroxy-4aH-eudesm-5-en-12-oic Acid g-Lactone/Naphtho[2,3-b]furan-2(3H)-one, 3a,5,6,7,8,8a,9,9a-octahydro-5,8a-dimethyl-3-methylene-, (3aR,5S,8aR,9aR)-/(3aR,5S,8aR,9aR)-5,8a-dimethyl-3-methylidene-3a,5,6,7,8,8a,9,9a-octahydronaphtho[2,3-b]furan-2(3H)-one/[3aR-(3aa,5b,8ab,9aa)]-3a,5,6,7,8,8a,9,9a-Octahydro-5,8a-dimethyl-3-methylenenaphtho[2,3-b]furan-2(3H)-one/Inula camphor/ALLANTOLACTONE/Helenin/HELENINE/ALANTOLACTONE/Elecampane camphor/ALANTOLACETONE/Eupatal/(3aR,5S,8aR,9aR)-5,8a-Dimethyl-3-methylene-3a,5,6,7,8,8a,9,9a-octahydronaphtho[2,3-b]furan-2(3H)-one/Alant camphor

IUPAC Name

(3aR,5S,8aR,9aR)-5,8a-dimethyl-3-methylidene-5,6,7,8,9,9a-hexahydro-3aH-benzo[f][1]benzofuran-2-one

Density

1.1±0.1 g/cm3

Solubility

Methanol; Ethyl Acetate

Flash Point

111.5±18.2 °C

Boiling Point

275.0±0.0 °C at 760 mmHg

Melting Point

78-79ºC

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2932200000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:546-43-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

30086361

Abstract

The lysosome is emerging as a central regulator of the autophagic process, which plays a critical role in tumor growth and chemoresistance. Alantolactone, which is a natural compound produced by Inula helenium, has been shown to induce apoptosis in numerous cancer types. However, the mechanism by which alantolactone regulates apoptosis is still poorly understood. In this work, we observed that alantolactone caused the accumulation of autophagosomes due to impaired autophagic degradation and substantially inhibited the activity and expression of CTSB/CTSD proteins that when depleted caused lysosomal dysfunction. Furthermore, we found that alantolactone inhibited the proliferation of pancreatic cancer cells in vitro and in vivo and enhanced the chemosensitivity of pancreatic cancer cells to oxaliplatin. In addition, a reduction in TFEB levels was a critical event in the apoptosis and cell death caused by alantolactone. Our data demonstrated that alantolactone, which impaired autophagic degradation, was a pharmacological inhibitor of autophagy in pancreatic cancer cells and markedly enhanced the chemosensitivity of pancreatic cancer cells to oxaliplatin.

Copyright © 2018 Elsevier Inc. All rights reserved.

KEYWORDS

Alantolactone; Apoptosis; Autophagy; Lysosome; Pancreatic cancer

Title

Alantolactone induces apoptosis and improves chemosensitivity of pancreatic cancer cells by impairment of autophagy-lysosome pathway via targeting TFEB.

Author

He R1, Shi X1, Zhou M1, Zhao Y1, Pan S1, Zhao C1, Guo X1, Wang M1, Li X2, Qin R3.

Publish date

2018 Oct 1

PMID

30015828

Abstract

Human breast cancer is a malignant type of cancer with high prevalence. In the present study, the anticancer effects of alantolactone, a sesquiterpene lactone, on the human breast cancer cell line MCF‑7 were investigated in vitro. The MCF‑7 cell morphology changed from diamond to round subsequent to treatment with alantolactone, and the cell viability reduced significantly compared with that of the control cells. Alantolactone induced apoptosis of MCF‑7 cells by regulating the protein expression levels of B‑cell lymphoma 2 (Bcl‑2), Bcl‑2‑associated X protein, p53, caspase‑3 and caspase‑12, which are associated with the apoptotic pathway, and suppressed colony formation and migration by regulating the protein expression of matrix metalloproteinase (MMP)‑2, MMP‑7 and MMP‑9. Cell signaling pathway analysis confirmed that alantolactone increased the phosphorylation of p38, and decreased the nuclear expression levels of p65 and nuclear factor erythroid 2‑related factor 2 (Nrf2), suggesting that the apoptosis‑promoting and migration‑suppressing effect of alantolactone may partially depend on regulating the p38 MAPK, NF‑κB and Nrf2 pathways. These results also suggested that alantolactone may become a potential therapeutic strategy for treating breast cancer.

Title

Alantolactone induces apoptosis and suppresses migration in MCF‑7 human breast cancer cells via the p38 MAPK, NF‑κB and Nrf2 signaling pathways.

Author

Liu J1, Liu M1, Wang S1, He Y1, Huo Y1, Yang Z1, Cao X1.

Publish date

2018 Oct

PMID

32064988

Abstract

Background: Inflammatory response plays a crucial role in the occurrence and development of diabetic nephropathy (DN). Drugs that carry anti-inflammatory effects have the potential to treat diabetic nephropathy. It’s reported that alantolactone (ALA), a natural product, has a variety of pharmacological effects against inflammation and oxidation. However, the specific effects of alantolactone on DN and the mechanisms underlying alantolactone remain elusive. Therefore, the present study aimed to probe whether ALA could mitigate inflammation as mediated by high glucose (HG) in NRK-52E cells and reduce renal injury caused by diabetic nephropathy.Materials and methods: The anti-inflammatory effect of ALA was evaluated in the present study using ELISA and RT-qPCR. Western blot and macrophage adhesion assay were then performed to confirm anti-macrophage adhesion and the protein expression of cell adhesion molecules. Finally, the effect of ALA and its underlying mechanism was evaluated in vivo.Results: Results showed that ALA curbed HG-stimulated expression of macrophage adhesion and pro-inflammatory cytokines in renal NRK-52E cells. In addition, both pro-inflammatory cytokines and NF-kappa B witnessed reduced expression or activity in oral administration with ALA in vivo, thus inhibiting the increase of serum creatinine and urea nitrogen (BUN) levels. This in consequence ameliorated fibrosis and stemmed pathological worsening of diabetic renal tissues.Conclusions: These findings suggest that ALA may hold promise in the treatment of DN, and importantly, the anti-inflammatory system may prove to be a new strategy to treat human DN.

KEYWORDS

Alantolactone; NF-kappa B; diabetic nephropathy; high glucose; inflammation

Title

Alantolactone mitigates renal injury induced by diabetes via inhibition of high glucose-mediated inflammatory response and macrophage infiltration.

Author

Zhu Y1, Ling Y2, Wang X1.

Publish date

2020 Apr


Description :

Alantolactone is a selective STAT3 inhibitor, with potent anticancer activity.