Oleocanthal


CAS No. : 289030-99-5

Oleocanthal,289030-99-5
Product Details
For research use only. Not Intended for Therapeutic Use!
Cat No:I013996
Synonyms:(-)-Oleocanthal; 2-(4-Hydroxyphenyl)ethyl (3S,4E)-4-formyl-3-(2-oxoethyl)hex-4-enoate
Molecular Formula:C17H20O5
Molecular Weight:304.342
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Cat No:I013996
Cas No:289030-99-5
Product-Name:Oleocanthal
IUPAC Name:2-(4-hydroxyphenyl)ethyl (E,3S)-4-formyl-3-(2-oxoethyl)hex-4-enoate
InChI:InChI=1S/C17H20O5/c1-2-14(12-19)15(7-9-18)11-17(21)22-10-8-13-3-5-16(20)6-4-13/h2-6,9,12,15,20H,7-8,10-11H2,1H3/b14-2-/t15-/m0/s1
InChIKey:VPOVFCBNUOUZGG-VAKDEWRISA-N
SMILES:CC=C(C=O)C(CC=O)CC(=O)OCCC1=CC=C(C=C1)O
Oleocanthal(cas 289030-99-5) is a compound of olive oil with potential use as anti-inflammatory and chemotherapeutic agents. Oleocanthal is a natural organic compound isolated from extra virgin olive oil. It is responsible for the slightly peppery "bite" of extra virgin olive oil. Oleocanthal is an tyrosol ester and its chemical structure is related to oleuropein that is also found in olive oil.
 
Oleocanthal has been found to be have anti-inflammatory and antioxidant properties. Similar to classical NSAIDs, it is a non-selective inhibitor of cyclooxygenase (COX). It is suggested that long-term consumption of small quantities of oleocanthal from olive oil may be responsible in part for the low incidence of heart disease associated with a Mediterranean diet.
1. Eur J Pharmacol. 2017 Sep 5;810:100-111. doi: 10.1016/j.ejphar.2017.06.019. Epub 2017 Jun 15.
The olive oil phenolic (-)-oleocanthal modulates estrogen receptor expression in luminal breast cancer in vitro and in vivo and synergizes with tamoxifen treatment.
Ayoub NM(1), Siddique AB(2), Ebrahim HY(2), Mohyeldin MM(2), El Sayed KA(2).
Author information:
(1)Department of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology, Irbid 22110, Jordan. Electronic address: nmayoub@just.edu.jo. (2)Department of Basic Pharmaceutical Sciences, School of Pharmacy, University of Louisiana at Monroe, Monroe, LA 71201, USA.
Luminal breast cancer represents a therapeutic challenge in terms of aggressive disease and emerging resistance to targeted therapy. (-)-Oleocanthal has demonstrated anticancer activity in multiple human cancers. The goal of this study was to explore the effect of (-)-oleocanthal treatment on growth of luminal breast cancer cells and to examine the effect of combination of (-)-oleocanthal with tamoxifen. Results showed that (-)-oleocanthal inhibited growth of BT-474, MCF-7, and T-47D human breast cancer cells in mitogen-free media with IC50 values of 32.7, 24.07, and 80.93µM, respectively. Similarly, (-)-oleocanthal suppressed growth of BT-474, MCF-7, and T-47D cells in 17β-estradiol-supplemented media with IC50 values of 22.28, 20.77, and 83.91µM, respectively. Combined (-)-oleocanthal and tamoxifen treatments resulted in a synergistic growth inhibition of BT-474, MCF-7, and T-47D cells with combination index values of 0.65, 0.61, and 0.53 for each cell line, respectively. In-silico docking studies indicated high degree of overlapping for the binding of (-)-oleocanthal and 17β-estradiol to estrogen receptors, while (-)-oleocanthal and tamoxifen have distinguished binding modes. Treatment with 5mg/kg or 10mg/kg (-)-oleocanthal resulted in 97% inhibition of tumor growth in orthotopic athymic mice bearing BT-474 tumor xenografts compared to vehicle-treated animals. (-)-Oleocanthal treatment reduced total levels of estrogen receptors in BT-474 cells both in vitro and in vivo. Collectively, (-)-oleocanthal showed a potential beneficial effect in suppressing growth of hormone-dependent breast cancer and improving sensitivity to tamoxifen treatment. These findings provide rational for evaluating the effect of (-)-oleocanthal in combination with endocrine treatments in luminal breast cancer.

2. Oncol Rep. 2017 Jan;37(1):483-491. doi: 10.3892/or.2016.5270. Epub 2016 Nov 23.
(-)-Oleocanthal exerts anti-melanoma activities and inhibits STAT3 signaling pathway.
Gu Y(1), Wang J(1), Peng L(1).
Author information:
(1)Department of Dermatology, Daqing Oilfield General Hospital, Saertu, Daqing, Heilongjiang 163001, P.R. China.
Tumor angiogenesis, growth and metastasis are three closely related processes. We therefore explored the effects of (-)-oleocanthal (OC) on the three processes in melanoma and investigated underlying mechanisms. In vitro, OC suppressed proliferation, migration, invasion and induced apoptosis in melanoma cells. In addition, OC inhibited proliferation, migration, invasion and tube formation in human umbilical vascular endothelial cells. In vivo, it exhibited potent activity in suppressing tumor growth in a subcutaneous xenograft model. Furthermore, OC suppressed proliferation and angiogenesis as measured by immunohistochemical staining of Ki-67 and CD31. In addition, OC was found to inhibit metastasis of melanoma in a lung metastasis model. Mechanistically, OC significantly suppressed signal transducer and activator of transcription 3 (STAT3) phosphorylation, decreased STAT3 nuclear localization and inhibited STAT3 transcriptional activity. OC also downregulated STAT3 target genes, including Mcl-1, Bcl-xL, MMP-2, MMP-9, VEGF, which are involved in apoptosis, invasion and angiogenesis of melanoma. These results support further investigation of OC as a potential anti-melanoma drug.

3. Oncotarget. 2016 Jul 12;7(28):43475-43491. doi: 10.18632/oncotarget.9782.
(-)-Oleocanthal inhibits growth and metastasis by blocking activation of STAT3 in human hepatocellular carcinoma.
Pei T(1), Meng Q(1), Han J(1), Sun H(1), Li L(1), Song R(1), Sun B(1), Pan S(1), Liang D(1), Liu L(1).
Author information:
(1)Key Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
We explored the anti-cancer capacity of (-)-oleocanthal in human hepatocellular carcinoma (HCC). (-)-Oleocanthal inhibited proliferation and cell cycle progression and induced apoptosis in HCC cells in vitro and suppressed tumor growth in an orthotopic HCC model. (-)-Oleocanthal also inhibited HCC cell migration and invasion in vitro and impeded HCC metastasis in an in vivo lung metastasis model. ( )-Oleocanthal acted by inhibiting epithelial-mesenchymal transition (EMT) through downregulation Twist, which is a direct target of STAT3. (-)-Oleocanthal also reduced STAT3 nuclear translocation and DNA binding activity, ultimately downregulating its downstream effectors, including the cell cycle protein Cyclin D1, the anti-apoptotic proteins Bcl-2 and survivin, and the invasion-related protein MMP 2. Overexpression of constitutively active STAT3 partly reversed the anti cancer effects of (-)-oleocanthal, which inhibited STAT3 activation by decreasing the activities of JAK1 and JAK2 and increasing the activity of SHP-1. These data suggest that (-)-oleocanthal may be a promising candidate for HCC treatment.

4. Mol Cell Oncol. 2015;2(4):e1006077.
(-)-Oleocanthal rapidly and selectively induces cancer cell death via lysosomal membrane permeabilization.
LeGendre O(1), Breslin PA(2), Foster DA(3).
Author information:
(1)Department of Biological Sciences; Hunter College of the City University of New York; New York, NY USA ; Department of Natural Sciences; LaGuardia Community College of the City University of New York; Long Island City, NY USA. (2)Rutgers University Department of Nutritional Sciences; New Brunswick, NJ USA ; Monell Chemical Senses Center; Philadelphia, PA USA. (3)Department of Biological Sciences; Hunter College of the City University of New York; New York, NY USA ; Department of Pharmacology; Weill-Cornell Medical College; New York, NY USA.
(-)-Oleocanthal (OC), a phenolic compound present in extra-virgin olive oil (EVOO), has been implicated in the health benefits associated with diets rich in EVOO. We investigated the effect of OC on human cancer cell lines in culture and found that OC induced cell death in all cancer cells examined as rapidly as 30 minutes after treatment in the absence of serum. OC treatment of non-transformed cells suppressed their proliferation but did not cause cell death. OC induced both primary necrotic and apoptotic cell death via induction of lysosomal membrane permeabilization (LMP). We provide evidence that OC promotes LMP by inhibiting acid sphingomyelinase (ASM) activity, which destabilizes the interaction between proteins required for lysosomal membrane stability. The data presented here indicate that cancer cells, which tend to have fragile lysosomal membranes compared to non-cancerous cells, are susceptible to cell death induced by lysosomotropic agents. Therefore, targeting lysosomal membrane stability represents a novel approach for the induction of cancer-specific cell death.
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