2. Cell Cycle/DNA Damage Cytoskeleton Apoptosis Metabolic Enzyme/Protease NF-κB Immunology/Inflammation
  3. Microtubule/Tubulin Bcl-2 Family Apoptosis MDM-2/p53 Mitochondrial Metabolism Reactive Oxygen Species (ROS)
  4. Bcl-2-IN-26

Bcl-2-IN-26 is an inhibitor targeting β-tubulin and BCL-2. Bcl-2-IN-26 disrupts the intracellular microtubule network and interferes with cell mitosis, inducing G2/M phase cell cycle arrest. Bcl-2-IN-26 suppresses antiapoptotic BCL-2 function via p53 upregulation, thereby triggering mitochondrial dysfunction, elevated ROS production and robust tumor cell apoptosis. Bcl-2-IN-26 can be used in lung cancer research[1]

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Bcl-2-IN-26

Bcl-2-IN-26 Chemical Structure

CAS No. : 3119834-80-6

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Bcl-2-IN-26 Related Antibodies

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Bcl-2 Bcl-xL Bcl-W Mcl-1 Bfl-1 Bcl-B Bax Bak Bim BNIP3 Bad

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Description

Bcl-2-IN-26 is an inhibitor targeting β-tubulin and BCL-2. Bcl-2-IN-26 disrupts the intracellular microtubule network and interferes with cell mitosis, inducing G2/M phase cell cycle arrest. Bcl-2-IN-26 suppresses antiapoptotic BCL-2 function via p53 upregulation, thereby triggering mitochondrial dysfunction, elevated ROS production and robust tumor cell apoptosis. Bcl-2-IN-26 can be used in lung cancer research[1]

IC50 & Target[1]

Bcl-2

 

β-Tubulin

 

In Vitro

Bcl-2-IN-26 (Compound 45) (72 h) exhibits potent inhibitory activity against NCI-H460 and A549 lung cancer cells with IC50s of 0.66 nM and 0.73 nM, respectively[1].
Bcl-2-IN-26 (1-5 nM; 24 h) blocks tubulin polymerization, disrupts microtubule networks and impairs mitosis in H460 cells[1].
Bcl-2-IN-26 (2-200 nM; 24 h) induces G2/M phase arrest and apoptosis in H460 cells in a dose-dependent manner[1].
Bcl-2-IN-26 (1-5 nM; 24 h) affects the expression of various apoptotic proteins, thereby inducing apoptosis in H460 cells[1].
Bcl-2-IN-26 (1-5 nM; 24 h) reduces mitochondrial transmembrane potential, induces dose-dependent ROS accumulation in H460 cells[1].
Bcl-2-IN-26 (1 nM; 48 h) triggers H460 cell death mainly by activating the p53 pathway to modulate BAX/BCL-2, with caspase activation only exerting weak auxiliary cytotoxic effects[1].
Bcl-2-IN-26 displays optimal antitumor activity owing to synergistic fluorine and alkene-mediated binding interactions with microtubules[1].

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

Bcl-2-IN-26 Related Antibodies

Cell Cycle Analysis[1]

Cell Line: NCI-H460 cells
Concentration: 2 nM, 5 nM, 100 nM, 200 nM
Incubation Time: 24 h
Result: Induced G2/M-phase arrest and apoptosis in H460 cells.

Immunofluorescence[1]

Cell Line: NCI-H460 cells
Concentration: 1 nM, 2 nM, 5 nM
Incubation Time: 24 h
Result: Induced irregular morphology in H460 cells.
Disrupted filamentous microtubule structures, loosened microtubules and blocked mitosis.
Showed the strongest green fluorescence, indicating a decrease in MMP.
Promoted intracellular ROS accumulation in H460 cells in a dose-dependent manner.

Western Blot Analysis[1]

Cell Line: NCI-H460 cells
Concentration: 1 nM, 2 nM, 5 nM
Incubation Time: 24 h
Result: Significantly upregulated the level of p53 protein expression in a dose-dependent manner.
Increased the level of pro-apoptotic BAX.
Blocked the anti-apoptotic function of BCL-2.
Activated caspase-3 and caspase-8 and triggers apoptosis in NCI-H460 cells.

Apoptosis Analysis[1]

Cell Line: NCI-H460 cells
Concentration: 1 nM
Incubation Time: 48 h
Result: Triggered cell death that pan-caspase inhibitors only weakly reversed.
Induced cell death that inhibiting the p53 pathway markedly rescued.

Western Blot Analysis[1]

Cell Line: NCI-H460 cells
Concentration: 1 nM
Incubation Time: 48 h
Result: Downregulated BAX and BCL-2 expression when p53 was inhibited.
In Vivo

Bcl-2-IN-26 (5-10 mg/kg; i.p.; every 3 days; for 15 days) effectively inhibits tumor growth without significant weight loss, indicating that Bcl-2-IN-26 has a good safety profile in the LLC homograft model in C57BL/6 mice[1].

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

Animal Model: 5-8-week-old male C57BL/6 mice were adaptively fed for one week before subcutaneous injection of 2.5 × 106 LLC cells[1].
Dosage: 5 mg/kg, 10 mg/kg
Administration: i.p., every 3 days, for 15 days
Result: Significantly inhibited tumor growth in mice.
Did not cause a significant decrease in the body weight of the mice.
Molecular Weight

386.35

Formula

C20H16F2N2O4
CAS No.
SMILES

FC1=CC(F)=CC(/C=C2NC(/C(NC\2=O)=C/C3=CC=C(COCC=C)O3)=O)=C1
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Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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Bcl-2-IN-26 Related Classifications

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Keywords:

Bcl-2-IN-263119834-80-6Microtubule/TubulinBcl-2 FamilyApoptosisMDM-2/p53Mitochondrial MetabolismReactive Oxygen Species (ROS)β-tubulinBCL-2H460 lung cancer cellsG2/Mcell cyclemitochondrial dysfunctionapoptosisLLC allograft mouse modelp53ROSInhibitorinhibitorinhibit

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