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3alpha-Hydroxytanshinone IIA

CAS# 97399-71-8

3alpha-Hydroxytanshinone IIA

Catalog No. BCN2496----Order now to get a substantial discount!

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Quality Control of 3alpha-Hydroxytanshinone IIA

Number of papers citing our products

Chemical structure

3alpha-Hydroxytanshinone IIA

3D structure

Chemical Properties of 3alpha-Hydroxytanshinone IIA

Cas No. 97399-71-8 SDF Download SDF
PubChem ID 14610644 Appearance Red powder
Formula C19H18O4 M.Wt 310.35
Type of Compound Diterpenoids Storage Desiccate at -20°C
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Chemical Name (7R)-7-hydroxy-1,6,6-trimethyl-8,9-dihydro-7H-naphtho[1,2-g][1]benzofuran-10,11-dione
SMILES CC1=COC2=C1C(=O)C(=O)C3=C2C=CC4=C3CCC(C4(C)C)O
Standard InChIKey PTDUBPDLRWKSBQ-CYBMUJFWSA-N
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of 3alpha-Hydroxytanshinone IIA

The roots of Salvia miltiorrhiza Bge.

Protocol of 3alpha-Hydroxytanshinone IIA

Structure Identification
Phytochemistry, 1985, 24(4):815-817.

Pigments from Salvia miltiorrhiza.[Reference: WebLink]


METHODS AND RESULTS:
Five new o-naphthaquinone diterpenes, tanshindiol A, tanshindiol B, tanshindiol C, nortanshinone and 3alpha-Hydroxytanshinone IIA, have been isolated from the roots of Salvia miltiorrhiza as minor components. Their relative stereochemistries have been established on the basis of spectral and chemical evidence.

3alpha-Hydroxytanshinone IIA Dilution Calculator

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3alpha-Hydroxytanshinone IIA Molarity Calculator

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Preparing Stock Solutions of 3alpha-Hydroxytanshinone IIA

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.2222 mL 16.1108 mL 32.2217 mL 64.4434 mL 80.5542 mL
5 mM 0.6444 mL 3.2222 mL 6.4443 mL 12.8887 mL 16.1108 mL
10 mM 0.3222 mL 1.6111 mL 3.2222 mL 6.4443 mL 8.0554 mL
50 mM 0.0644 mL 0.3222 mL 0.6444 mL 1.2889 mL 1.6111 mL
100 mM 0.0322 mL 0.1611 mL 0.3222 mL 0.6444 mL 0.8055 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on 3alpha-Hydroxytanshinone IIA

Sodium Tanshinone IIA Sulfonate Prevents Radiation-Induced Toxicity in H9c2 Cardiomyocytes.[Pubmed:28386289]

Evid Based Complement Alternat Med. 2017;2017:4537974.

The present study was designed to elucidate the key parameters associated with X-ray radiation induced oxidative stress and the effects of STS on X-ray-induced toxicity in H9c2 cardiomyocytes. Cytotoxicity of STS and radiation was assessed by MTT. Antioxidant activity was evaluated by SOD and MDA. Apoptosis was measured by the flow cytometry, Hoechst 33258, clonogenic survival assay, and western blot. It was found that the cell viability of H9c2 cells exposed to X-ray radiation was significantly decreased in a dose-dependent manner and was associated with cell cycle arrest at the G0/G1 phase as well as apoptosis. STS treatment significantly reversed the morphological changes, attenuated radiation-induced apoptosis, and improved the antioxidant activity in the H9c2 cells. STS significantly increased the Bcl-2 and Bcl-2/Bax levels and decreased the Bax and caspase-3 levels, compared with the cells treated with radiation alone. STS treatment also resulted in a significant increase in p38-MAPK activation. STS could protect the cells from X-ray-induced cell cycle arrest, oxidative stress, and apoptosis. Therefore, we suggest the STS could be useful for the treatment of radiation-induced cardiovascular injury.

Fludarabine resistance mediated by aminoglycoside-3'-phosphotransferase-IIa and the structurally related eukaryotic cAMP-dependent protein kinase.[Pubmed:28373209]

FASEB J. 2017 Jul;31(7):3007-3017.

While working with G418-resistant stably transfected cells, we realized the neomycin resistance (NeoR) gene, which encodes the aminoglycoside-3'-phosphotransferase-IIa [APH(3')-IIa], also confers resistance to the nucleoside analog fludarabine. Fludarabine is a cytostatic drug widely used in the treatment of hematologic and solid tumors, as well as in the conditioning of patients before transplantation of hematopoietic progenitors. We present evidence that NeoR-transfected cells do not incorporate fludarabine, thus avoiding DNA damage caused by the drug, evidenced by a lack of FANCD2 monoubiquitination and impaired apoptosis. A screening of other nucleoside analogs revealed that APH(3')-IIa only protects against ATP purine analogs. Moreover, APH(3')-IIa ATPase activity is inhibited by fludarabine monophosphate, suggesting that APH(3')-IIa blocks fludarabine incorporation into DNA by dephosphorylating its active fludarabine triphosphate form. Furthermore, overexpression of the catalytic subunit of the eukaryotic kinase PKA, which is structurally related to APHs, also provides resistance to fludarabine, anticipating its putative utility as a response marker to the drug. Our results preclude the use of Neo marker plasmids in the study of purine analogs and unveils a new resistance mechanism against these chemotherapeuticals.-Sanchez-Carrera, D., Bravo-Navas, S., Cabezon, E., Arechaga, I., Cabezas, M., Yanez, L., Pipaon, C. Fludarabine resistance mediated by aminoglycoside-3'-phosphotransferase-IIa and the structurally related eukaryotic cAMP-dependent protein kinase.

The MOBILE Study-A Phase IIa Enriched Enrollment Randomized Withdrawal Trial to Assess the Analgesic Efficacy and Safety of ASP8477, a Fatty Acid Amide Hydrolase Inhibitor, in Patients with Peripheral Neuropathic Pain.[Pubmed:28383710]

Pain Med. 2017 Dec 1;18(12):2388-2400.

Objective: To evaluate the analgesic efficacy and safety of ASP8477 in patients with peripheral neuropathic pain (PNP). Design: Enriched enrollment randomized withdrawal. Setting: Centers in Poland (four), Czech Republic (six), and the United Kingdom (two). Subjects: Patients aged 18 years or older with PNP resulting from painful diabetic peripheral neuropathy or postherpetic neuralgia. Methods: A four-week screening period followed by a single-blind period (six-day dose titration and three-week maintenance period with ASP8477 [20/30 mg BID]). Treatment responders (defined as a >/=30% decrease in the mean average daily pain intensity during the last three days of the single-blind period) were stratified by disease and randomized to receive placebo or continue ASP8477 during a three-week, double-blind, randomized withdrawal period. The primary end point was change in mean 24-hour average numeric pain rating scale (NPRS) from baseline to end of double-blind period. Results: Among 132 patients who enrolled, 116 entered the single-blind period and 63 (ASP8477, N = 31; placebo, N = 32) completed the double-blind period. There was no difference in mean 24-hour average NPRS score (P = 0.644) or in time-to-treatment failure (P = 0.485) between ASP8477 and placebo. During the single-blind period, 57.8% of patients were treatment responders. ASP8477 was well tolerated. During the single-blind period, 22% of patients experienced at least one treatment-related adverse event (TEAE); during the double-blind period, 8% in the ASP8477 arm and 18% in the placebo arm experienced at least one TEAE. Conclusions: ASP8477 was well tolerated in patients with PNP; however, ASP8477 did not demonstrate a significant treatment difference compared with placebo.

Randomized study between radical surgery and radiotherapy for the treatment of stage IB-IIA cervical cancer: 20-year update.[Pubmed:28382797]

J Gynecol Oncol. 2017 May;28(3):e34.

OBJECTIVE: Stage IB-IIA cervical carcinoma can be equally cured either by radical surgery or radiotherapy (RT). Albeit such policies show the same efficacy, they carry a different morbidity. This is an update after 20 years of a previously published randomized trial of RT vs. surgery in the treatment of stage IB-IIA cervical cancers to assess long-term survival and morbidity and the different pattern of relapse between the 2 modalities. METHODS: Between September 1986 and December 1991, women referred for a newly diagnosed stage IB and IIA cervical carcinoma were randomized to radical surgery or RT. The primary outcome measures were long-term survival and complications rate. The secondary outcome was recurrence of the disease. RESULTS: Three-hundred forty-three eligible women were randomized: 172 to radical surgery and 171 to external RT. Minimum follow-up was 19 years. Thirty-three patients (10%) died of intercurrent disease (31 cases) or fatal complications (2 cases). Twenty-year overall survival is 72% and 77% in the 2 treatment groups (p=0.280), respectively. As a whole, 94 recurrences (28%) were observed. Median time to relapse was 13.5 (surgery group) and 11.5 months (radiotherapy group) (p=0.100), respectively. Multivariate analysis confirms that risk factors for survival are histotype (p=0.020), tumor diameter (p=0.008), and lymph node status (p<0.001). CONCLUSION: The results of the present study seem to suggest that there is no treatment of choice for early stage cervical carcinoma in terms of survival. Long term follow-up confirms that the best treatment for the individual patient should take into account clinical factors such as menopausal status, comorbidities, histological type, and tumor diameter.

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