RA-VCAS# 64725-24-2 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 64725-24-2 | SDF | Download SDF |
PubChem ID | 13361282 | Appearance | Powder |
Formula | C40H48N6O9 | M.Wt | 756.9 |
Type of Compound | Alkaloids | Storage | Desiccate at -20°C |
Synonyms | Deoxybouvardin | ||
Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
Chemical Name | (1S,4R,7S,10S,13S,16S)-24-hydroxy-10-[(4-methoxyphenyl)methyl]-4,7,9,13,15,29-hexamethyl-22-oxa-3,6,9,12,15,29-hexazatetracyclo[14.12.2.218,21.123,27]tritriaconta-18,20,23,25,27(31),32-hexaene-2,5,8,11,14,30-hexone | ||
SMILES | CC1C(=O)NC(C(=O)N(C(C(=O)NC(C(=O)N(C2CC3=CC=C(C=C3)OC4=C(C=CC(=C4)CC(C(=O)N1)N(C2=O)C)O)C)C)CC5=CC=C(C=C5)OC)C)C | ||
Standard InChIKey | VXVGFMUNENQGFW-LZQLRFBTSA-N | ||
Standard InChI | InChI=1S/C40H48N6O9/c1-22-35(48)42-23(2)38(51)44(4)30(18-25-8-13-28(54-7)14-9-25)37(50)43-24(3)39(52)46(6)32-19-26-10-15-29(16-11-26)55-34-21-27(12-17-33(34)47)20-31(36(49)41-22)45(5)40(32)53/h8-17,21-24,30-32,47H,18-20H2,1-7H3,(H,41,49)(H,42,48)(H,43,50)/t22-,23+,24+,30+,31+,32+/m1/s1 | ||
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. RA-V is an potential anti-angiogenic agent, exhibits anti-angiogenic activities in HUVEC and HMEC-1 cell lines with changes in function of these endothelial cells. 2. RA-V has anti-cancer activity, is a potential anti-metastatic agent in breast cancer, and likely acts via PI3K/AKT and NF-κB signaling pathways in both ER-positive and ER-negative breast cancer cells. |
Targets | FAK | MMP(e.g.TIMP) | EGFR | PI3K | Akt | NF-kB | Estrogen receptor | PDK | ERK | JNK | p38MAPK | Progestogen receptor |
RA-V Dilution Calculator
RA-V Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 1.3212 mL | 6.6059 mL | 13.2118 mL | 26.4236 mL | 33.0295 mL |
5 mM | 0.2642 mL | 1.3212 mL | 2.6424 mL | 5.2847 mL | 6.6059 mL |
10 mM | 0.1321 mL | 0.6606 mL | 1.3212 mL | 2.6424 mL | 3.3029 mL |
50 mM | 0.0264 mL | 0.1321 mL | 0.2642 mL | 0.5285 mL | 0.6606 mL |
100 mM | 0.0132 mL | 0.0661 mL | 0.1321 mL | 0.2642 mL | 0.3303 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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Cyclopeptide RA-V inhibits angiogenesis by down-regulating ERK1/2 phosphorylation in HUVEC and HMEC-1 endothelial cells.[Pubmed:21518338]
Br J Pharmacol. 2011 Dec;164(7):1883-98.
BACKGROUND AND PURPOSE: Anti-angiogenic agents have recently become one of the major adjuvants for cancer therapy. A cyclopeptide, RA-V, has been shown to have anti-tumour activities. Its in vitro anti-angiogenic activities were evaluated in the present study, and the underlying mechanisms were also assessed. EXPERIMENTAL APPROACH: Two endothelial cell lines, human umbilical vein endothelial cells (HUVEC) and human microvascular endothelial cells (HMEC-1), were used. The effects of RA-V on the proliferation, cell cycle phase distribution, migration, tube formation and adhesion were assessed. Western blots and real-time PCR were employed to examine the protein and mRNA expression of relevant molecules. KEY RESULTS: RA-V inhibited HUVEC and HMEC-1 proliferation dose-dependently with IC(50) values of 1.42 and 4.0 nM respectively. RA-V inhibited migration and tube formation of endothelial cells as well as adhesion to extracellular matrix proteins. RA-V treatment down-regulated the protein and mRNA expression of matrix metalloproteinase-2. Regarding intracellular signal transduction, RA-V interfered with the activation of ERK1/2 in both cell lines. Furthermore, RA-V significantly decreased the phosphorylation of JNK in HUVEC whereas, in HMEC-1, p38 MAPK was decreased. CONCLUSIONS AND IMPLICATIONS: RA-V exhibited anti-angiogenic activities in HUVEC and HMEC-1 cell lines with changes in function of these endothelial cells. The underlying mechanisms of action involved the ERK1/2 signalling pathway. However, RA-V may regulate different signalling pathways in different endothelial cells. These findings suggest that RA-V has the potential to be further developed as an anti-angiogenic agent.
Cyclopeptide RA-V inhibits cell adhesion and invasion in both estrogen receptor positive and negative breast cancer cells via PI3K/AKT and NF-kappaB signaling pathways.[Pubmed:25953046]
Biochim Biophys Acta. 2015 Aug;1853(8):1827-40.
Cyclopeptide RA-V has potent anti-tumor and anti-angiogenic activities, but its potential anti-metastatic activity is unknown. Cancer cells acquire invasive ability to degrade and adhere to extracellular matrix (ECM), allowing them to migrate to adjacent tissues and ultimately metastasize. Hence, the present study aimed to investigate the effects of RA-V on cell adhesion, migration, invasion and matrix degradation, and its underlying mechanism in two human breast cancer cell lines MCF-7 (ER-positive) and MDA-MB-231 (ER-negative). Our results demonstrated that RA-V (12.5 nM) can significantly inhibit breast cancer cell adhesion and migration via interfering cofilin signaling and chemokine receptors involved in cell migration. RA-V reduced the expressions of vascular intracellular adhesion molecule (VCAM), intracellular adhesion molecule (ICAM), focal adhesion kinase (FAK) and integrins. The activities and expressions of matrix metalloproteinases (MMPs), tissue inhibitors of matrix metalloproteinases (TIMPs) and urokinase-type of plasminogen activator (uPA) were also inhibited by RA-V. Furthermore, RA-V inhibits the expressions of EGFR, PI3K/AKT and NF-kappaB signaling molecules, and reduces the binding of beta-estradiol to ER via affecting binding ability of ER in MCF-7 cells. RA-V inhibits breast cancer cell migration, adhesion and ECM degradation in vitro, implying that RA-V is a potential anti-metastatic agent in breast cancer, and likely acts via PI3K/AKT and NF-kappaB signaling pathways in both ER-positive and ER-negative breast cancer cells.
Plant cyclopeptide RA-V kills human breast cancer cells by inducing mitochondria-mediated apoptosis through blocking PDK1-AKT interaction.[Pubmed:23274515]
Toxicol Appl Pharmacol. 2013 Feb 15;267(1):95-103.
In the present paper, we examined the effects of a natural cyclopeptide RA-V on human breast cancer cells and the underlying mechanisms. RA-V significantly inhibited the growth of human breast cancer MCF-7, MDA-MB-231 cells and murine breast cancer 4T1 cells. In addition, RA-V triggered mitochondrial apoptotic pathway which was indicated by the loss of mitochondrial membrane potential, the release of cytochrome c, and the activation of caspase cascade. Further study showed that RA-V dramatically inhibited phosphorylation of AKT and 3-phosphoinositide dependent protein kinase 1 (PDK1) in MCF-7 cells. Moreover, RA-V disrupted the interaction between PDK1 and AKT in MCF-7 cells. Furthermore, RA-V-induced apoptosis could be enhanced by phosphatidylinositol 3-kinase inhibitor or attenuated by over-expression of AKT in all the three kinds of breast cancer cells. Taken together, this study shows that RA-V, which can induce mitochondria-mediated apoptosis, exerts strong anti-tumor activity against human breast cancer. The underlying anti-cancer mechanism of RA-V is related to the blockage of the interaction between PDK1 and AKT.