AlismolCAS# 87827-55-2 |
2D Structure
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Cas No. | 87827-55-2 | SDF | Download SDF |
PubChem ID | 137357 | Appearance | Oil |
Formula | C15H24O | M.Wt | 220.4 |
Type of Compound | Sesquiterpenoids | Storage | Desiccate at -20°C |
Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
Chemical Name | (1R,3aS,8aS)-1-methyl-4-methylidene-7-propan-2-yl-2,3,3a,5,6,8a-hexahydroazulen-1-ol | ||
SMILES | CC(C)C1=CC2C(CCC2(C)O)C(=C)CC1 | ||
Standard InChIKey | BUPJOLXWQXEJSQ-QLFBSQMISA-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. |
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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. |
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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. |
Description | 1. Alismol acts primarily on nerve terminals and inhibits their responses to electrical stimulation by interfering with NAd release. 2. Alismol inhibits mainly Ca2+ influx through a voltage-dependent Ca2+ channel. 3. Alismol holds great promise for use in chemopreventive and chemotherapeutic strategies. 4. Alismol has antihypertensive action. 5. Alismol decreases cardiac output, heart rate and left ventricular pressure, but it increases coronary flow, it has been used for the prevention of anginal attacks. 6. Alismol has inhibitory effect to MMP3 expression and nitric oxide produced in microglial cells. |
Targets | Calcium Channel | Potassium Channel | PI3K | Akt | ERK | JNK | Caspase | MMP(e.g.TIMP) |
Alismol Dilution Calculator
Alismol Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 4.5372 mL | 22.686 mL | 45.3721 mL | 90.7441 mL | 113.4301 mL |
5 mM | 0.9074 mL | 4.5372 mL | 9.0744 mL | 18.1488 mL | 22.686 mL |
10 mM | 0.4537 mL | 2.2686 mL | 4.5372 mL | 9.0744 mL | 11.343 mL |
50 mM | 0.0907 mL | 0.4537 mL | 0.9074 mL | 1.8149 mL | 2.2686 mL |
100 mM | 0.0454 mL | 0.2269 mL | 0.4537 mL | 0.9074 mL | 1.1343 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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Effect of alismol on adrenergic mechanism in isolated rabbit ear artery.[Pubmed:3404764]
Jpn J Pharmacol. 1988 Apr;46(4):331-5.
Effects of Alismol, a sesquiterpenoid isolated from the rhyzome of Alisma orientale, on adrenergic mechanisms were examined in the isolated rabbit ear artery. Alismol (10(-6) to 10(-4) M) inhibited the contraction of isolated rabbit ear artery by electrical stimulation of the perivascular nerves. The inhibition was concentration-dependent; at a concentration of 10(-4) M, the inhibition was 90% (n = 8). Treatment with 10(-4) M Alismol inhibited the increase in 3H-noradrenaline (3H-NAd) release induced by electrical stimulation by 63 +/- 6%. Alismol at 10(-4) M did not affect the neuronal uptake of 3H-NAd in the artery. Alismol at 10(-4) M slightly inhibited contractions induced by exogenously administered NAd. These results demonstrate that Alismol inhibits the adrenergic neuro-effector mechanisms in rabbit ear artery, and they suggest that Alismol acts primarily on nerve terminals and inhibits their responses to electrical stimulation by interfering with NAd release.
In Vitro Morphological Assessment of Apoptosis Induced by Antiproliferative Constituents from the Rhizomes of Curcuma zedoaria.[Pubmed:23762112]
Evid Based Complement Alternat Med. 2013;2013:257108.
Bioassay-guided isolation of the active hexane fractions of Curcuma zedoaria led to the identification of five pure compounds, namely, curzerenone (1), neocurdione (2), curdione (3), Alismol (4), and zederone (5) and a mixture of sterols, namely, campesterol (6), stigmasterol (7), and beta -sitosterol (8). Alismol has never been reported to be present in Curcuma zedoaria. All isolated compounds except (3) were evaluated for their cytotoxic activity against MCF-7, Ca Ski, and HCT-116 cancer cell lines and noncancer human fibroblast cell line (MRC-5) using neutral red cytotoxicity assay. Curzerenone and Alismol significantly inhibited cell proliferation in human cancer cell lines MCF-7, Ca Ski, and HCT-116 in a dose-dependent manner. Cytological observations by an inverted phase contrast microscope and Hoechst 33342/PI dual-staining assay showed typical apoptotic morphology of cancer cells upon treatment with curzerenone and Alismol. Both compounds induce apoptosis through the activation of caspase-3. It can thus be suggested that curzerenone and Alismol are modulated by apoptosis via caspase-3 signalling pathway. The findings of the present study support the use of Curcuma zedoaria rhizomes in traditional medicine for the treatment of cancer-related diseases. Thus, two naturally occurring sesquiterpenoids, curzerenone and Alismol, hold great promise for use in chemopreventive and chemotherapeutic strategies.
Effects of alismol isolated from Alismatis Rhizoma on calcium-induced contraction in the rabbit thoracic aorta.[Pubmed:3657386]
Life Sci. 1987 Oct 12;41(15):1845-52.
We examined the inhibitory effects of Alismol, a sesquiterpenoid isolated from Alismatis Rhizoma, on vascular contractions induced by high concentrations of K+ and Ca2+, and on 45Ca2+ retention in normal and in high K+-containing medium. Alismol affected neither the resting tension nor the 45Ca2+ retention in normal medium, but it inhibited sustained contraction and increased 45Ca2+ retention induced by high K+ concentrations. Alismol did not affect norepinephrine-induced contractions in normal medium, nor phasic contractions in Ca2+-free medium. These results suggested that Alismol inhibited mainly Ca2+ influx through a voltage-dependent Ca2+ channel.