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Art. -Nr.: HY-N7892A

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(±)-Forbesione

(±)-Forbesione, a potential apoptosis inducer, is a racemate of Forbesione (HY-N7892). (±)-Forbesione inhibits proliferation of cancer cells. (±)-Forbesione can be used for cancer research.

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CAS. Nr.: 667914-50-3
Formel: C₂₈H₃₂O₆
Molecular Weight:464.55

Speicherung:

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

(±)-Forbesione Chemical Structure

CAS. Nr.: 667914-50-3

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Biologische Aktivität
- Beschreibung
- In Vitro
- In Vivo
Chemical Information
Reinheit & Dokumentation
Verweise
Calculators
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Bioz

Biologische Aktivität

Beschreibung

(±)-Forbesione, a potential apoptosis inducer, is a racemate of Forbesione (HY-N7892). (±)-Forbesione inhibits proliferation of cancer cells. (±)-Forbesione can be used for cancer research^[1].

In Vitro

(±)-Forbesione (range of concentrations; 24 h) exhibits low micromolar antiproliferative activity against HepG2, A549, and U251 cells, with IC₅₀ values of 4.07 μM, 3.58 μM, and 8.57 μM, respectively^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Cycle Analysis^[1]

Cell Line:

Ham-1 cholangiocarcinoma cells
Concentration:

0.5 µM; 1 µM; 2 µM; 4 µM; 8 µM
Incubation Time:

24 h
Result:

Induced concentration-dependent S-phase cell cycle arrest (P<0.01).
Reduced the proportion of cells in the G₀/G₁ (P<0.05) and G₂/M (P<0.05) phases.
Increased the percentage of cells in the sub-G₁ fraction (apoptotic cells) significantly in a concentration-dependent manner (P<0.01).

Apoptosis Analysis^[1]

Cell Line:

Ham-1 cholangiocarcinoma cells
Concentration:

2 µM; 4 µM; 8 µM; 16 µM
Incubation Time:

24 h
Result:

Induced bright green, condensed, and fragmented chromatin, which are hallmarks of apoptosis, in treated cells, while untreated cells showed uniformly green-stained, normal nuclei.

Apoptosis Analysis^[1]

Cell Line:

Ham-1 cholangiocarcinoma cells
Concentration:

2 µM; 4 µM; 8 µM; 16 µM; 32 μM
Incubation Time:

6, 24, 48 h
Result:

Increased the percentage of apoptotic cells in a concentration- and time-dependent manner.
Resulted in 50.75% (P<0.01), 55.57% (P<0.001), and 64.43% (P<0.001) apoptotic cells at 6, 24, and 48 h respectively when treated with 32 µM.

Western Blot Analysis^[1]

Cell Line:

Ham-1 cholangiocarcinoma cells
Concentration:

2 µM; 4 µM; 8 µM
Incubation Time:

24 h
Result:

Significantly decreased protein expression of cyclin E (P<0.01), cyclin A (P<0.05), and cyclin-dependent kinase 2 (Cdk2) (P<0.01).
Significantly increased protein expression of p21 (P<0.05) and p27 (P<0.05) compared to control cells.\nIncreased protein expression of Fas (P<0.05), Fas-associated death domain (FADD) (P<0.05), and activated caspase-3 (P<0.05) in the death receptor pathway.
Decreased protein expression of procaspase-8 (P<0.05) and procaspase-3 (P<0.01) in the death receptor pathway.
Increased protein expression of B-cell lymphoma-2-like protein 4 (Bax) (P<0.05), activated caspase-9 (P<0.05), and activated caspase-3 (P<0.05) in the mitochondrial pathway.
Decreased protein expression of B-cell lymphoma-2 (Bcl-2) (P<0.05), procaspase-9 (P<0.05), and procaspase-3 (P<0.01) in the mitochondrial pathway.
Increased protein expression of activated caspase-12 (P<0.05), activated caspase-9 (P<0.05), and activated caspase-3 (P<0.05) in the endoplasmic reticulum pathway.
Decreased protein expression of procaspase-12 (P<0.05), procaspase-9 (P<0.05), and procaspase-3 (P<0.01) in the endoplasmic reticulum pathway.\nSignificantly decreased protein expression of NF-κB/p65 (P<0.01) compared to control cells.
Significantly increased protein expression of inhibitor of κB-α (IκB-α) (P<0.05) compared to control cells.\nSignificantly decreased protein expression of cytokeratin 19 (CK19) (P<0.01) compared to control cells.
Significantly decreased protein expression of proliferating cell nuclear antigen (PCNA) (P<0.05) compared to control cells.

Apoptosis Analysis^[3]

Cell Line:

human cholangiocarcinoma KKU-100 cells
Concentration:

0.25 µM; 0.5 µM; 1 µM; 2 μM; 1 μM (combined with 0.025 μM Doxorubicin)
Incubation Time:

48 h
Result:

Increased apoptosis in KKU-100 cells in a dose-dependent manner, with the highest single-agent dose (2 μM) inducing ~32% apoptotic cells.
Induced ~75% apoptotic cells when combined with 0.025 μM Doxorubicin, which was significantly higher than either single agent alone.

Western Blot Analysis^[3]

Cell Line:

human cholangiocarcinoma KKU-100 cells
Concentration:

0.25 μM; 0.5 μM; 1 μM (single agent); 0.25 μM + 0.006 μM Doxorubicin (C1); 0.5 μM + 0.012 μM Doxorubicin (C2); 1 μM + 0.025 μM Doxorubicin (C3)
Incubation Time:

48 h
Result:

Decreased Bcl-2 expression (0.27-fold at 1 μM) and increased Bax expression (2.06-fold at 1 μM) as a single agent, leading to a Bax/Bcl-2 ratio of 1.63; the C3 combination further decreased Bcl-2 to 0.10-fold and increased Bax to 3.24-fold, resulting in a Bax/Bcl-2 ratio of 12.00.
Decreased survivin (0.35-fold at 1 μM), procaspase-9 (0.70-fold at 1 μM), and procaspase-3 (0.76-fold at 1 μM) while increasing activated caspase-9 (42.00-fold at 1 μM) and activated caspase-3 (42.00-fold at 1 μM) as a single agent; the C3 combination enhanced these effects, reducing procaspase-9 and procaspase-3 to 0-fold and increasing activated caspase-9 and caspase-3 to 64.00-fold and 54.00-fold, respectively.
Increased IκB-α (1.15-fold at 1 μM) and decreased pIκB-α (0.14-fold at 1 μM) and NF-κB/p65 (0.12-fold at 1 μM) as a single agent; the C3 combination further increased IκB-α to 1.21-fold and decreased pIκB-α and NF-κB/p65 to 0.01-fold each.
Decreased MRP1 expression (0.71-fold at 1 μM) as a single agent, while the C3 combination reduced MRP1 to 0.34-fold, a significantly greater effect than single-agent treatment.

In Vivo

Animal Model:

Syrian hamsters (male, 6-8 weeks old, intradermal injection of 2.5×10⁵ Ham-1 cholangiocarcinoma cells)^[1]
Dosage:

50 mg/kg
Administration:

p.o.; daily; 4 weeks
Result:

Reduced tumor volume (P<0.01) and mean tumor weight from 0.54 g (control) to 0.27 g (P<0.001).
Significantly decreased relative CK19 mRNA expression in tumor tissues (P<0.05).
Significantly increased relative Bax, Apaf-1, caspase-9, and caspase-3 mRNA expression in tumor tissues (P<0.05).
Significantly decreased expression of CK19 (P=0.036), PCNA (P=0.032), cyclin A (P=0.028), and Bcl-2 (P=0.039) in tumor tissues via immunohistochemical analysis.
Significantly increased expression of Bax (P=0.039), caspase-9 (P=0.028), and caspase-3 (P=0.039) in tumor tissues via immunohistochemical analysis.
Increased body weight (P<0.001), food intake (P<0.001), and water intake (P<0.05) in treated hamsters.
Caused no significant histopathological changes in liver, kidney, or stomach, and no changes in serum liver (ALT, ALP) or kidney (BUN, creatinine) function markers.

Chemical Information

CAS. Nr. 667914-50-3
Molecular Weight 464.55
Formel C₂₈H₃₂O₆
SMILES

C/C(C)=C\CC1(O2)C(C(C3)C2(C)C)(OC4=C(C(O)=C5)C/C=C(C)\C)C(C(C4=C5O)=O)=CC3C1=O
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]. Zhang X, et al. Garcinia xanthones as orally active antitumor agents. J Med Chem. 2013;56(1):276-292. [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.

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