Desethylamiodarone
Desethylamiodarone (N-Desethylamiodarone; LB 33020) is the major active metabolite of Amiodarone (HY-14187) generated via CYP3A4 metabolism. Desethylamiodarone downregulates p‑Akt, p‑Bad and Bcl‑2, upregulates Bax, promotes mitochondrial release of cytochrome c, activates caspase‑3 and cleaves PARP‑1, thereby inducing cell cycle arrest and apoptosis. Desethylamiodarone can be used in cervical cancer-related research.
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- CAS. Nr.: 83409-32-9
- Formel: C23H25I2NO3
- Molecular Weight:617.26
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
Beschreibung
IC50 & Target
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CYP3A4 |
Caspase-3 |
PARP-1 |
Bax |
Bcl-2 |
bad |
Akt |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| HEK293 | EC50 |
33 nM
Compound: 4, dE-Ami
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Antagonist activity at rat TAAR1 expressed in HEK293 cells assessed as intracellular cAMP level
Antagonist activity at rat TAAR1 expressed in HEK293 cells assessed as intracellular cAMP level
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[PMID: 18752950] |
| LLC-PK1 | IC50 |
15.4 μM
Compound: Desethylamiodarone
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TP_TRANSPORTER: inhibition of Daunorubicin transepithelial transport (basal to apical) (Daunorubicin: 0.035 uM) in MDR1-expressing LLC-PK1 cells
TP_TRANSPORTER: inhibition of Daunorubicin transepithelial transport (basal to apical) (Daunorubicin: 0.035 uM) in MDR1-expressing LLC-PK1 cells
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[PMID: 11231118] |
| LLC-PK1 | IC50 |
25.2 μM
Compound: Desethylamiodarone
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TP_TRANSPORTER: inhibition of Digoxin transepithelial transport (basal to apical) (Digoxin: 0.025 uM) in MDR1-expressing LLC-PK1 cells
TP_TRANSPORTER: inhibition of Digoxin transepithelial transport (basal to apical) (Digoxin: 0.025 uM) in MDR1-expressing LLC-PK1 cells
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[PMID: 11231118] |
In Vitro
Desethylamiodarone (DEA) (2.5-10 μM; 24-72 h) reduces the viability of human cervical cancer HeLa cells in a dose- and time-dependent manner[1].
Desethylamiodarone (0.5-2 μM; 7 days) inhibits colony formation of human cervical cancer HeLa cells in a dose-dependent manner[1].
Desethylamiodarone (2.5-5 μM; 24 h) inhibits the PI3K-Akt pathway in human cervical cancer HeLa cells in a dose-dependent manner by reducing the phosphorylation levels of Akt and its downstream target Bad; it also regulates the expression of apoptosis-related proteins in human cervical cancer HeLa cells in a dose-dependent manner: downregulating Bcl-2, upregulating Bax, inducing cytochrome c release, and activating the cleavage of caspase-3 and PARP-1[1].
Desethylamiodarone (5-10 μM; 24 h) induces apoptosis-related nuclear morphological changes (pyknosis and fragmentation) in human cervical cancer HeLa cells; it also induces apoptosis in human cervical cancer HeLa cells in a dose-dependent manner[1].
Desethylamiodarone (5 μM; 24 h) induces G0/G1 cell cycle arrest in human cervical cancer HeLa cells[1].
Desethylamiodarone (2.5-12.5 μg/mL; 1-4 days) exerts strong direct cytotoxicity against human thyroid cell line SGHTL-34 cultured in vitro, with an EC50 of 6.8 μg/mL at 24 h. It reduces cell numbers through cell destruction rather than decreasing cell adhesion, and induces vacuolization after 4 days of exposure[2].
Desethylamiodarone exhibits strong direct cytotoxicity against primary human retro-orbital fibroblasts in vitro, and a reduction in cell number is detected via protein content assay after 4 days of exposure[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HeLa human cervical cancer cells
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Concentration:2.5, 5, 7.5, 10 μM
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Incubation Time:24 h, 48 h, 72 h
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Result:Inhibited HeLa cell viability in a dose- and time-dependent manner.
Caused dose-dependent reductions in total viable cell counts over time, with 10 μM causing a decrease in viable cell numbers after 24 h that continued through 72 h.
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Cell Line:HeLa human cervical cancer cells
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Concentration:0.5, 1, 1.5, 2 μM
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Incubation Time:7 days
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Result:Strongly reduced colony formation in a dose-dependent manner.
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Cell Line:HeLa human cervical cancer cells
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Concentration:5, 10 μM
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Incubation Time:24 h
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Result:Induced characteristic apoptotic nuclear morphology, including condensed and fragmented nuclei, as indicated by bright fluorescent staining of affected nuclei.\nIncreased total apoptosis in a dose-dependent manner.
Increased total apoptosis to ~33% (23% early apoptotic, ~10% late apoptotic) at 5 μM, compared to ~13% in controls.
Increased total apoptosis to ~61% (16% early apoptotic, ~45% late apoptotic) at 10 μM.
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Cell Line:HeLa human cervical cancer cells
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Concentration:5 μM
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Incubation Time:24 h
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Result:Increased the percentage of cells in G0/G1 phase to ~70.5% (from ~55.5% in controls).
Decreased the percentage of cells in S phase to ~22.1% (from ~34.0% in controls).
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Cell Line:HeLa human cervical cancer cells
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Concentration:2.5, 5 μM
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Incubation Time:24 h
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Result:Dose‑dependently diminished Akt and Bad phosphorylation while leaving total Akt and Bad protein levels unaltered.
Decreased phospho‑Akt to ~70 % of control and phospho‑Bad to ~75 % of control at 2.5 μM.
Lowered phospho‑Akt to ~35 % of control and phospho‑Bad to ~20 % of control at 5 μM.
Dose‑dependently suppressed anti‑apoptotic Bcl‑2, elevated pro‑apoptotic Bax, triggered mitochondrial‑to‑cytosolic cytochrome c release, induced caspase‑3 cleavage‑mediated activation, and promoted cleavage of PARP‑1 (caspase‑3 downstream substrate).
Attenuated Bcl‑2 to ~25 % of control, raised Bax, cytosolic cytochrome c, cleaved caspase‑3 and cleaved PARP‑1 by ~100 % relative to control at 5 μM.
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Cell Line:immortalized functional human thyrocyte line SGHTL-34
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Concentration:2.5, 7.5, 12.5, 6.8 μg/mL
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Incubation Time:4 days
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Result:Markedly reduced SGHTL-34 cell number as measured by DNA and protein content.
Induced vacuole formation in SGHTL-34 cells after 4-day incubation with 7.5 μg/mL.
Had cytotoxic effect unmodified by co-incubation with T3 (up to 0.75 μg/mL) at 2.5 μg/mL or 7.5 μg/mL over 4 days.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Swiss mice (adult female, 20-25 g)[3]
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Dosage:100 mg/kg (generated via amiodarone metabolism)
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Administration:i.p.; single dose; 30 min prior to testing
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Result:Significantly elevated brain concentrations when coadministered with oxcarbazepine compared to amiodarone alone.
Significantly elevated brain concentrations when coadministered with pregabalin compared to amiodarone alone.
Did not significantly alter brain concentrations when coadministered with lamotrigine compared to amiodarone alone.
Chemical Information
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CAS. Nr. 83409-32-9
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Molecular Weight 617.26
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Formel C23H25I2NO3
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SMILES
O=C(C1=CC(I)=C(C(I)=C1)OCCNCC)C2=C(OC3=CC=CC=C23)CCCC
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Synonyms
N-Desethylamiodarone; LB 33020
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
Desethylamiodarone Related Classifications
HY-122423 Related Classifications
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Keywords
- Desethylamiodarone
- 83409-32-9
- N-Desethylamiodarone
- LB 33020
- LB33020
- LB 33020
- LB-33020
- Drug Metabolite
- Cytochrome P450
- Akt
- Bcl-2 Family
- Caspase
- PARP
- Apoptosis
- phosphorylated Akt
- Bax
- proliferation
- HeLa human cervical cancer cells
- blood-brain barrier
- phosphorylated Bad
- apoptosis
- Bcl-2
- PI3K-Akt signaling
- SGHTL-34 human thyrocytes
- Inhibitor
- inhibitor
- inhibit