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Art. -Nr.: HY-114802

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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.

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CAS. Nr.: 468083-84-3
Formel: C₂₇H₃₈O₂
Molecular Weight:394.59

Speicherung:

Please store the product under the recommended conditions in the Certificate of Analysis.

O-1663 Chemical Structure

CAS. Nr.: 468083-84-3

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Reinheit & Dokumentation
Verweise
Calculators
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target

^[1]

CB2

Alle Cannabinoid Receptor Isoform-spezifische Produkte anzeigen :

In Vitro

Anti-cancerOxidative StressAutophagyApoptosis

Anti-cancer

Oxidative Stress

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].

Anti-cancer

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].

Autophagy

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].

Oxidative Stress

O-1663 (0.5-1.5 μM; 2 days) significantly induces ROS production in human MDA-MB231 breast cancer cells^[1].

Apoptosis

Anti-cancer

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.

Cell Proliferation Assay^[1]

Cell Line:

human MDA-MB231 breast cancer cells
Concentration:

1 μM; 4 μM
Incubation Time:

2 days
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).

Cell Proliferation Assay^[1]

Cell Line:

mouse 4T1 breast cancer cells
Concentration:

1 μM; 4 μM
Incubation Time:

2 days
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.

Cell Invasion Assay^[1]

Cell Line:

human MDA-MB231 breast cancer cells
Concentration:

1 μM
Incubation Time:

3 days
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.

Western Blot Analysis^[1]

Cell Line:

human MDA-MB231 breast cancer cells, mouse 4T1 breast cancer cells
Concentration:

1 μM; 1.5 μM
Incubation Time:

2 days (LC3-II); 3 days (Id1/Id2, LC3-II)
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.

Apoptosis Analysis^[1]

Cell Line:

human MDA-MB231 breast cancer cells
Concentration:

1.5 μM
Incubation Time:

2 days
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.

In Vivo

Anti-cancer

O-1663 (0.1-1 mg/kg; i.p.; once daily; for 14 consecutive days) potently inhibits breast cancer metastasis in BALB/c mice^[1].
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.

Animal Model:

BALB/c (6-8 week old female; i.v. injection of 2 × 10⁴ mouse 4T1 breast cancer cells)^[1]
Dosage:

0.1 mg/kg; 0.5 mg/kg; 1 mg/kg
Administration:

i.p.; daily; 14 days
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.

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]
Dosage:

0.5 mg/kg; 1 mg/kg
Administration:

i.p.; daily; 14 days
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.

Related Protocols :

Chemical Information

CAS. Nr. 468083-84-3
Molecular Weight 394.59
Formel C₂₇H₃₈O₂
SMILES

OC1=CC(C(C)(CCCCCC)C)=CC(O)=C1C2CCC(CC2)C3=CC=CC=C3
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

Please store the product under the recommended conditions in the Certificate of Analysis.

Reinheit & Dokumentation

Handling Instructions (2659 KB)

Verweise

[1]. Murase R, et al. Targeting multiple cannabinoid anti-tumour pathways with a resorcinol derivative leads to inhibition of advanced stages of breast cancer. British journal of pharmacology. 2014 Oct;171(19):4464-77. [Content Brief]

Calculators

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Bioz

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Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Reinheit & Dokumentation
Verweise

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O-1663

Alle Cannabinoid Receptor Isoform-spezifische Produkte anzeigen