Gigantol isomer-1

For research use only. Not for therapeutic Use.

  • CAT Number: R072515
  • CAS Number: 67884-30-4
  • Molecular Formula: C16H18O4
  • Molecular Weight: 274.31
  • Purity: ≥95%
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Gigantol isomer-1 is a bibenzyl compound derived from Dendrobium nobile. Gigantol isomer-1 shows promising therapeutic potential against cancer cells. Gigantol isomer-1 is a novel inhibitor of the Wnt/β-catenin pathway.
Gigantol isomer-1 decreases the level of phosphorylated LRP6 and cytosolic β-catenin in HEK293 cells. In breast cancer MDA-MB-231 and MDA-MB-468 cells, treatment with Gigantol isomer-1 reduces the level of phosphorylated LRP6[1]. Gigantol isomer-1 significantly inhibits the proliferation and induces apoptosis of the HepG2 cells. Gigantol isomer-1 at concentrations of 1, 40 and 150 μM markedly decreases the cell viability by 11.7, 30.0 and 56.4% at 24 h and 21.1, 66.8 and 85.5% at 48 h, respectively. The IC50 value is 9.30 μM[2].
LDD and Gigantol isomer-1 (25–100 mg/kg, p.o.) significantly increase the hot-plate latency in comparison to vehicle-treated mice and decreased carrageenaninduced inflammation in rats[2].


Catalog Number R072515
CAS Number 67884-30-4
Synonyms

5-[2-(3-hydroxy-5-methoxyphenyl)ethyl]-2-methoxyphenol

Molecular Formula C16H18O4
Purity ≥95%
InChI InChI=1S/C16H18O4/c1-19-14-8-12(7-13(17)10-14)4-3-11-5-6-16(20-2)15(18)9-11/h5-10,17-18H,3-4H2,1-2H3
InChIKey SDXKZPQOVUDXIY-UHFFFAOYSA-N
SMILES COC1=C(C=C(C=C1)CCC2=CC(=CC(=C2)OC)O)O
Reference

[1]. Yu S, et al. Gigantol inhibits Wnt/β-catenin signaling and exhibits anticancer activity in breast cancer cells. BMC Complement Altern Med. 2018 Feb 14;18(1):59.
 [Content Brief]

[2]. Chen H, et al. Gigantol attenuates the proliferation of human liver cancer HepG2 cells through the PI3K/Akt/NF-κB signaling pathway. Oncol Rep. 2017 Feb;37(2):865-870.
 [Content Brief]

[3]. Déciga-Campos M, et al. Antinociceptive and anti-inflammatory effects of compounds isolated from Scaphyglottis livida and Maxillaria densa. J Ethnopharmacol. 2007 Nov 1;114(2):161-8.
 [Content Brief]

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