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β-thujaplicin DNA Methyltransferase inhibitor

Name: β-thujaplicin
Brand: Selleck Chemicals
SKU: S4771
Rating: 5 (1 reviews)

Cat.No.S4771

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.

Chemical Structure

Molecular Weight: 164.20

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Quality Control

Batch: Purity: 99.82%

99.82

Related Targets	HDAC JAK BET Histone Methyltransferase PKC PARP HIF PRMT EZH2 AMPK
Other DNA Methyltransferase Inhibitors	RG108 SGI-1027 Zebularine (NSC 309132) GSK3685032 Gamma-Oryzanol CM272 Bobcat339 DC-05 2'-Deoxy-5-Fluorocytidine GSK-3484862

Chemical Information, Storage & Stability

Molecular Weight	164.20	Formula	C₁₀H₁₂O₂	Storage (From the date of receipt)	3 years-20°Cpowder
CAS No.	499-44-5	Download SDF		Storage of Stock Solutions	1 year-80°Cin solvent 1 month-20°Cin solvent
Synonyms	Hinokitiol, 4-Isopropyltropolone			Smiles	CC(C)C1=CC(=O)C(=CC=C1)O

Solubility

In vitro
Batch:

DMSO : 32 mg/mL (194.88 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Molarity Calculator

Mass	Concentration	Volume	Molecular Weight
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Dilution Calculator Molecular Weight Calculator

In vivo Batch:
Homogeneous suspension	CMC-NA	≥5mg/ml	Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
Homogeneous suspension	CMC-NA	≥5mg/ml	Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
Homogeneous suspension	CMC-NA	≥5mg/ml	Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)

Dosage: mg/kg Average weight of animals: g Dosing volume per animal:μL Number of animals:

Step 2: Enter the in vivo formulation (This is only the calculator, not formulation. Please contact us first if there is no in vivo formulation at the solubility Section.)

% DMSO + % + % Tween 80 + % ddH₂O

%DMSO+ %

Calculation results:

Working concentration: mg/ml;

Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH₂O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.

Mechanism of Action

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) signalling 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 tumour growth, potentially through the attenuation of tumorigenicity, and induces DNA damage and autophagy to suppress tumour 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] https://pubmed.ncbi.nlm.nih.gov/25105411/ [2] https://pubmed.ncbi.nlm.nih.gov/25449038/

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