β-thujaplicin

β-Thujaplicin (β-TH, Hinokitiol, 4-Isopropyltropolone) is a toxic tropolone derivative present in the heartwood of western red cedar (Thuja plicata) and is used as a preservative and antimicrobial additive in a number of commercial goods. Hinokitiol is a component of essential oils isolated from Chymacyparis obtusa, reduces Nrf2 expression, and decreases DNMT1 and UHRF1 mRNA and protein expression, with anti-infective, anti-oxidative, and anti-tumor activities.

Product information

CAS Number: 499-44-5

Molecular Weight: 164.20

Formula: C10H12O2

Synonym:

β-Thujaplicin

Chemical Name: 2-hydroxy-6-(propan-2-yl)cyclohepta-2,4,6-trien-1-one

Smiles: CC(C)C1C=CC=C(O)C(=O)C=1

InChiKey: FUWUEFKEXZQKKA-UHFFFAOYSA-N

InChi: InChI=1S/C10H12O2/c1-7(2)8-4-3-5-9(11)10(12)6-8/h3-7H,1-2H3,(H,11,12)

Technical Data

Appearance: Solid Power

Purity: ≥98% (or refer to the Certificate of Analysis)

Solubility: Solubility (25°C). 32 mg/mL(194.88 mM).

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis

Storage Condition: Dry, dark and -20 ^oC for 1 year or refer to the Certificate of Analysis.

Shelf Life: ≥12 months if stored properly.

Stock Solution Storage: 0 - 4 ^oC for 1 month or refer to the Certificate of Analysis.

Drug Formulation: To be determined

HS Tariff Code: 382200

How to use

In Vitro:

In lung cancer cells, hinokitiol inhibits cell proliferation by inducing the p53-independent DNA damage response, autophagy (not apoptosis), S-phase cell cycle arrest, and senescence. Hinokitiol induces autophagy in lung adenocarcinoma cells but not in human lung stromal fibroblasts. It induces cellular senescence in both human lung cancer cells and lung stromal fibroblasts. Treatment with hinokitiol reveals a concentration-dependent inhibition of migration of B16-F10 melanoma cells. It appears to achieve this effect by reducing the expression of MMP-1 and by suppressing the phosphorylation of mitogen- activated protein kinase (MAPK) signaling molecules such as extracellular signal-regulated kinase (ERK) 1/2, p38 MAPK and c-Jun N-terminal kinases (JNK). On the other hand, hinokitiol treatment reverses IκB-α degradation and inhibits the phosphorylation of p65 nuclear factor kappa B (NF-κB) and cJun in B16-F10 cells. In addition, hinokitiol suppresses the translocation of p65 NF-κB from the cytosol to the nucleus, suggesting reduced NF-κB activation.

In Vivo:

Hinokitiol reduces tumor growth, potentially through the attenuation of tumorigenicity, and induces DNA damage and autophagy to suppress tumor progression. In vivo study demonstrates that hinokitiol treatment significantly reduces the total number of mouse lung metastatic nodules and improves histological alterations in B16-F10 injected C57BL/6 mice.

References:

1. Ouyang WC, et al. Hinokitiol suppresses cancer stemness and oncogenicity in glioma stem cells by Nrf2 regulation. Cancer Chemother Pharmacol. 2017 Aug;80(2):411-419.
2. Seo JS, et al. Hinokitiol induces DNA demethylation via DNMT1 and UHRF1 inhibition in colon cancer cells. BMC Cell Biol. 2017 Feb 27;18(1):14.

Products are for research use only. Not for human use.