1. Apoptosis
  2. Apoptosis
  3. Apoptosis inducer 52

Apoptosis inducer 52 is a derivative of flutamide that induces apoptosis in prostate cancer cells. Apoptosis inducer 52 promotes apoptosis by activating both intrinsic and extrinsic apoptotic pathways, without generating reactive oxygen species (ROS). Apoptosis inducer 52 triggers caspase 3/7 activity and the externalization of phosphatidylserine, leading to cell cycle arrest at the G0/G1 phase. Apoptosis inducer 52 can be used for the research of androgen receptor (AR)-dependent and -independent prostate cancers and leukemia.

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Apoptosis inducer 52

Apoptosis inducer 52 Chemical Structure

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Description

Apoptosis inducer 52 is a derivative of flutamide that induces apoptosis in prostate cancer cells. Apoptosis inducer 52 promotes apoptosis by activating both intrinsic and extrinsic apoptotic pathways, without generating reactive oxygen species (ROS). Apoptosis inducer 52 triggers caspase 3/7 activity and the externalization of phosphatidylserine, leading to cell cycle arrest at the G0/G1 phase. Apoptosis inducer 52 can be used for the research of androgen receptor (AR)-dependent and -independent prostate cancers and leukemia[1].

In Vitro

Apoptosis inducer 52 (compoun a5) (1-100 μM; 48 h; LNCaP) inhibits LNCaP and nonmalignant HaCaT cells with IC50 values of 8.89 µM and 28.71 µM, respectively[1].
Apoptosis inducer 52 displays a remarkable antiproliferative activity toward the K-562 cell line from the leukemia subpanel[1].
Apoptosis inducer 52 (10 μM; 24-48 h; LNCaP) induces apoptosis in a time‐dependent.[1].
Apoptosis inducer 52 (10 μM; 48 h; LNCaP) arrests cell cycle in G0/G1 phase[1].
Apoptosis inducer 52 (10 μM; 48 h; LNCaP) increases expression of caspase 3, 8, 9 and upregulates BAX[1].
Apoptosis inducer 52 (10 μM; 12-24 h; LNCaP) marginally increases ROS production. The result suggest that apoptosis induction by Apoptosis inducer 52 may be ROS-independent[1].

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

Cell Viability Assay[1]

Cell Line: LNCaP and HaCaT cells
Concentration: 1, 2.5, 5, 10, 25, 50, 100 μM
Incubation Time: 48 h
Result: Cell viability decreased in a dose-dependent manner.

Apoptosis Analysis[1]

Cell Line: LNCaP
Concentration: 10 μM
Incubation Time: 24, 48 h
Result: The ratio of apoptotic cells increased significantly at the end of the 48 h.
Caspase 3/7 activity increased and phosphatidylserine externalization was observed.

Cell Cycle Analysis[1]

Cell Line: LNCaP
Concentration: 10 μM
Incubation Time: 48 h
Result: Inhibited the cell cycle progression by arresting the cells in the G0/G1 phase.

Western Blot Analysis[1]

Cell Line: LNCaP
Concentration: 10 μM
Incubation Time: 48 h
Result: Expression levels of pro‐caspase 3, pro‐caspase 9, caspase 3, caspase 9, caspase 8 increased, and BAX levels were upregulated.
Molecular Weight

546.32

Formula

C22H15F6N3O2Se

SMILES

O=C(C1=CC=CN=C1NC2=CC=CC(C(F)(F)F)=C2)[Se]CC(NC3=CC=CC(C(F)(F)F)=C3)=O

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Room temperature in continental US; may vary elsewhere.

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

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Apoptosis inducer 52
Cat. No.:
HY-179124
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