O-1663
O-1663 is a full agonist of cannabinoid receptor 2 (CB2 receptor). O-1663 stimulates the production of ROS, downregulates Id1, and induces autophagy and apoptosis in breast cancer cells. O-1663 inhibits the proliferation, invasion and metastasis of breast cancer cells. O-1663 prolongs the survival of models with advanced metastatic breast cancer. O-1663 can be used for the research of metastatic breast cancer.
For research use only. We do not sell to patients.
- CAS No.: 468083-84-3
- Formula: C27H38O2
- Molecular Weight:394.59
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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CB2 |
O-1663 (1-4 μM; 2 days) potently inhibits the proliferation/survival of human MDA-MB231 and 4T1 breast cancer cells, with IC50 values of 0.85 μM and 0.83 μM, respectively. This effect is partially mediated by CB2 receptor activation and ROS production[1].
O-1663 (1 μM; 3 days) potently inhibits the invasion of human MDA-MB231 breast cancer cells, with an IC50 of 0.6 μM[1].
O-1663 inhibits the proliferation and viability of human MDA-MB231-luc-D3H2LN breast cancer cells, with an IC50 value of 1.0 μM[1].
O-1663 (1-1.5 μM; 2-3 days) downregulates Id1 expression and upregulates Id2 expression in human MDA-MB231 and mouse 4T1 breast cancer cells, and also stimulates autophagy in MDA-MB231 cells by upregulating LC3-II expression to a level comparable to that of THC[1].
O-1663 (0.5-1.5 μM; 2 days) significantly induces ROS production in human MDA-MB231 breast cancer cells[1].
O-1663 (1.5 μM; 2 days) induces apoptosis in human MDA-MB231 breast cancer cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human MDA-MB231 breast cancer cells
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Concentration:1 μM; 4 μM
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Incubation Time:2 days
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Result:Inhibited MDA-MB231 cell proliferation/viability with an IC50 of 0.85 μM.
Reversed inhibitory effect was observed with α-tocopherol and partially reversed by CB2 antagonist SR144528 (HY-13439), but not by CB1 antagonist SR141716A (HY-14137).
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Cell Line:mouse 4T1 breast cancer cells
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Concentration:1 μM; 4 μM
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Incubation Time:2 days
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Result:Inhibited 4T1 cell proliferation/viability with an IC50 of 0.83 μM.
Reversed inhibitory effect was observed with α-tocopherol and partially reversed by CB2 antagonist SR144528, but not by CB1 antagonist SR141716A.
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Cell Line:human MDA-MB231 breast cancer cells
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Concentration:1 μM
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Incubation Time:3 days
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Result:Inhibited MDA-MB231 cell invasion with an IC50 of 0.6 μM, which was 1.7-fold more potent than CBD.
Partially reversed inhibitory effect was observed with CB2 antagonist SR144528.
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Cell Line:human MDA-MB231 breast cancer cells, mouse 4T1 breast cancer cells
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Concentration:1 μM; 1.5 μM
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Incubation Time:2 days (LC3-II); 3 days (Id1/Id2, LC3-II)
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Result:Almost completely down-regulated Id1 expression in both MDA-MB231 and 4T1 cells.
More potently up-regulated Id2 expression in 4T1 cells compared to CBD.
Up-regulated LC3-II expression to a similar extent as THC, producing a ~150% increase over vehicle control, which was significantly higher than the moderate increase induced by CBD.
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Cell Line:human MDA-MB231 breast cancer cells
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Concentration:1.5 μM
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Incubation Time:2 days
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Result:Induced apoptosis in ~18% of MDA-MB231 cells, which was significantly higher than the minimal apoptosis induced by CBD and higher than the ~9% apoptosis induced by THC.
O-1663 (0.5-1 mg/kg; i.p.; daily administration; for 6 consecutive weeks) potently inhibits the metastasis of human MDA-MB231 breast cancer cells in athymic nu/nu mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c (6-8 week old female; i.v. injection of 2 × 104 mouse 4T1 breast cancer cells)[1]
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Dosage:0.1 mg/kg; 0.5 mg/kg; 1 mg/kg
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Administration:i.p.; daily; 14 days
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Result:Exhibited 2.3-fold more potency than CBD at inhibiting total metastasis, with an EC50 of 0.13 mg/kg.
Showed 7.0-fold more potency than CBD at inhibiting lung metastatic foci ≥ 2 mm, with an EC50 of 0.02 mg/kg.
Reduced total metastasis to ~15% relative to vehicle at 1 mg/kg.
Reduced lung metastatic foci ≥ 2 mm to near 0 at 1 mg/kg.
Had anti-metastatic activity partially reversed by co-administration with CB2 receptor antagonist SR144528.
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Animal Model:BALB/c (6-8 week old female; i.v. injection of 2 × 104 mouse 4T1 breast cancer cells, treatment initiated 7 days post-injection when lung metastatic foci were established)[1]
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Dosage:0.5 mg/kg; 1 mg/kg
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Administration:i.p.; daily; 14 days
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Result:Reduced total metastasis to ~45% relative to vehicle at 0.5 mg/kg.
Reduced lung metastatic foci ≥2 mm to ~1 at 0.5 mg/kg.
Reduced total metastasis to ~30% relative to vehicle at 1 mg/kg.
Reduced lung metastatic foci ≥ 2 mm to near 0 at 1 mg/kg.
Produced a median survival increase of 30 days.
Allowed 50% of treated mice to remain alive with no disease progression at 2 months, with 20% having few visible lung metastatic foci.
Chemical Information
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CAS No. 468083-84-3
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Molecular Weight 394.59
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Formula C27H38O2
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SMILES
OC1=CC(C(C)(CCCCCC)C)=CC(O)=C1C2CCC(CC2)C3=CC=CC=C3
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
O-1663 Related Classifications
HY-114802 Related Classifications
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