AmarogentinCAS# 21018-84-8 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 21018-84-8 | SDF | Download SDF |
| PubChem ID | 115149 | Appearance | Yellowish powder |
| Formula | C29H30O13 | M.Wt | 586.54 |
| Type of Compound | Iridoids | Storage | Desiccate at -20°C |
| Solubility | DMSO : 130 mg/mL (221.64 mM; Need ultrasonic) | ||
| Chemical Name | [(2S,3R,4S,5S,6R)-2-[[(3S,4R,4aS)-4-ethenyl-8-oxo-4,4a,5,6-tetrahydro-3H-pyrano[3,4-c]pyran-3-yl]oxy]-4,5-dihydroxy-6-(hydroxymethyl)oxan-3-yl] 2,4-dihydroxy-6-(3-hydroxyphenyl)benzoate | ||
| SMILES | C=CC1C2CCOC(=O)C2=COC1OC3C(C(C(C(O3)CO)O)O)OC(=O)C4=C(C=C(C=C4C5=CC(=CC=C5)O)O)O | ||
| Standard InChIKey | DBOVHQOUSDWAPQ-WTONXPSSSA-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. Amarogentin incorporated in liposomes or niosomes may have clinical application in the treatment of leishmaniasis. 2. Amarogentin plays cemopreventive/therapeutic role during liver carcinogenesis through modulation of cell cycle and apoptosis. 3. Amarogentin prevents platelet activation through the inhibition of PLC γ2-PKC cascade and MAPK pathway, it may offer therapeutic potential for preventing or treating thromboembolic disorders. |
| Targets | COX | PKC | MAPK | p53 | p21 | Caspase | Bcl-2/Bax | PARP | c-Myc |
Amarogentin Dilution Calculator
Amarogentin Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.7049 mL | 8.5246 mL | 17.0491 mL | 34.0983 mL | 42.6228 mL |
| 5 mM | 0.341 mL | 1.7049 mL | 3.4098 mL | 6.8197 mL | 8.5246 mL |
| 10 mM | 0.1705 mL | 0.8525 mL | 1.7049 mL | 3.4098 mL | 4.2623 mL |
| 50 mM | 0.0341 mL | 0.1705 mL | 0.341 mL | 0.682 mL | 0.8525 mL |
| 100 mM | 0.017 mL | 0.0852 mL | 0.1705 mL | 0.341 mL | 0.4262 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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Prevention of liver carcinogenesis by amarogentin through modulation of G1/S cell cycle check point and induction of apoptosis.[Pubmed:22948180]
Carcinogenesis. 2012 Dec;33(12):2424-31.
Amarogentin, a secoiridoid glycoside, is an active component of the medicinal plant Swertia chirata. In this study, chemopreventive and chemotherapeutic actions of Amarogentin were evaluated in a carbon tetrachloride (CCl(4))/N-nitrosodiethylamine (NDEA)-induced liver carcinogenesis mouse model system during continuous and posttreatment schedule. Better survival, no toxicity and increased body weight were noted in Amarogentin-treated mice. Reduction in proliferation and increase in apoptosis frequency were evident in Amarogentin-treated groups. In carcinogen control group moderate dysplasia, severe dysplasia and hepatocellular carcinoma were evident at 10th, 20th and 30th week, respectively. Amarogentin was found to prevent progression of liver carcinogenesis at mild dysplastic stage. Exposure to CCl(4)/NDEA resulted in upregulation of ppRb807/811, cyclinD1 and cdc25A at 10th week and additional activation of cMyc and mdm2 along with downregulation of LIMD1, p53 and p21 at 20th week. This was followed by activation of ppRb567 and downregulation of Rbsp3 at 30th week. Prevention of carcinogenesis by Amarogentin in both groups might be due to cumulative upregulation of LIMD1, RBSP3, p16 and downregulation of cdc25A at 10th week along with activation of p53 and p21 and downregulation of ppRb807/811 and ppRb567 at 20th week, followed by downregulation of cyclinD1, cMyc and mdm2 at 30th week. During carcinogenesis reduction of apoptosis was evident since 20th week. However, Amarogentin treatment could significantly induce apoptosis through upregulation of the Bax-Bcl2 ratio, activation of caspase-3 and poly ADP ribose polymerase cleavage. This is the first report of chemopreventive/therapeutic role of Amarogentin during liver carcinogenesis through modulation of cell cycle and apoptosis.
Amarogentin, a secoiridoid glycoside, abrogates platelet activation through PLC gamma 2-PKC and MAPK pathways.[Pubmed:24868545]
Biomed Res Int. 2014;2014:728019.
Amarogentin, an active principle of Gentiana lutea, possess antitumorigenic, antidiabetic, and antioxidative properties. Activation of platelets is associated with intravascular thrombosis and cardiovascular diseases. The present study examined the effects of Amarogentin on platelet activation. Amarogentin treatment (15~60 muM) inhibited platelet aggregation induced by collagen, but not thrombin, arachidonic acid, and U46619. Amarogentin inhibited collagen-induced phosphorylation of phospholipase C (PLC) gamma2, protein kinase C (PKC), and mitogen-activated protein kinases (MAPKs). It also inhibits in vivo thrombus formation in mice. In addition, neither the guanylate cyclase inhibitor ODQ nor the adenylate cyclase inhibitor SQ22536 affected the Amarogentin-mediated inhibition of platelet aggregation, which suggests that Amarogentin does not regulate the levels of cyclic AMP and cyclic GMP. In conclusion, Amarogentin prevents platelet activation through the inhibition of PLC gamma2-PKC cascade and MAPK pathway. Our findings suggest that Amarogentin may offer therapeutic potential for preventing or treating thromboembolic disorders.
Evaluation of the in-vivo activity and toxicity of amarogentin, an antileishmanial agent, in both liposomal and niosomal forms.[Pubmed:10590280]
J Antimicrob Chemother. 1999 Dec;44(6):791-4.
The antileishmanial property of Amarogentin, a secoiridoid glycoside isolated from the Indian medicinal plant Swertia chirata, was examined in a hamster model of experimental leishmaniasis. The therapeutic efficacy of Amarogentin was evaluated in free and two different vesicular forms, liposomes and niosomes. The Amarogentin in both liposomal and niosomal forms was found to be a more active leishmanicidal agent than the free Amarogentin; and the niosomal form was found to be more efficacious than the liposomal form at the same membrane microviscosity level. Toxicity studies involving blood pathology, histological staining of tissues and specific enzyme levels related to normal liver function showed no toxicity. Hence, Amarogentin incorporated in liposomes or niosomes may have clinical application in the treatment of leishmaniasis.
