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Cat. No.: 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 No.: 468083-84-3
Formule: C₂₇H₃₈O₂
Masse moléculaire:394.59

Stockage:

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

O-1663 Chemical Structure

CAS No.: 468083-84-3

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Use of MCE Products

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

Activité biologique
- Description
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Pureté et documentation
Références
Calculators
Help & FAQs
Classifications
Bioz

Activité biologique

Description

IC₅₀ & Target

^[1]

CB2

Voir tous les produits spécifiques à Isoform Cannabinoid Receptor :

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 No. 468083-84-3
Masse moléculaire 394.59
Formule C₂₇H₃₈O₂
SMILES

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

Room temperature in continental US; may vary elsewhere.
Stockage

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

Pureté et documentation

Instruction de manipulation (2659 KB)

Références

[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]

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Activité biologique
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- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Pureté et documentation
Références

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O-1663

Voir tous les produits spécifiques à Isoform Cannabinoid Receptor