2. Cell Cycle/DNA Damage Cytoskeleton Apoptosis Epigenetics
  3. Microtubule/Tubulin Apoptosis Bcl-2 Family Caspase PARP
  4. ICD inducer-2

ICD inducer-2 is a immunogenic cell death inducer. ICD inducer-2 binds to the colchicine binding site on tubulin to inhibit tubulin polymerization. ICD inducer-2 exhibits broad-spectrum antiproliferative activity across multiple cancer cell lines. ICD inducer-2 inhibits cells migration, causes G2/M phase and induces apoptosis. ICD inducer-2 promotes infiltration of CD4+ and CD8+ T cells into the tumor microenvironment. ICD inducer-2 downregulates antiapoptotic protein Bcl-2, upregulates proapoptotic proteins Bax and Bim-1, and increases cleaved caspase 3, cleaved caspase 9, and cleaved PARP levels. ICD inducer-2 overcomes paclitaxel resistance in xenograft models and achieves tumor growth inhibition. ICD inducer-2 can be used for the research of cancer, such as lung carcinoma.

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ICD inducer-2

ICD inducer-2 Chemical Structure

CAS No. : 3069681-35-9

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ICD inducer-2 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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PARP PARP1 PARP2 PARP3 PARP4 TNKS1/PARP5A TNKS2/PARP5B PARP7 PARP10 PARP14 PARP15 PARP12 PARP16

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Description

ICD inducer-2 is a immunogenic cell death inducer. ICD inducer-2 binds to the colchicine binding site on tubulin to inhibit tubulin polymerization. ICD inducer-2 exhibits broad-spectrum antiproliferative activity across multiple cancer cell lines. ICD inducer-2 inhibits cells migration, causes G2/M phase and induces apoptosis. ICD inducer-2 promotes infiltration of CD4+ and CD8+ T cells into the tumor microenvironment. ICD inducer-2 downregulates antiapoptotic protein Bcl-2, upregulates proapoptotic proteins Bax and Bim-1, and increases cleaved caspase 3, cleaved caspase 9, and cleaved PARP levels. ICD inducer-2 overcomes paclitaxel resistance in xenograft models and achieves tumor growth inhibition. ICD inducer-2 can be used for the research of cancer, such as lung carcinoma[1].

IC50 & Target[1]

Bcl-2

 

Bax

 

Bim

 

Caspase 9

 

Caspase 3

 

In Vitro

ICD inducer-2 (Compound 17) (1.25-5 μM; 60 min) inhibits purified tubulin polymerization in a dose-dependent manner[1].
ICD inducer-2 (0.2-25 μM; 2 h) binds to the colchicine-binding site on tubulin in A549 cells[1].
ICD inducer-2 (10-20 nM; 48 h) disrupts the microtubule network in A549 cells at 10 and 20 nM[1].
ICD inducer-2 (20-80 nM; 12 h) potently induces ICD in A549 cells[1].
ICD inducer-2 (8-64 nM; 12-24 h) exhibits immunostimulatory potential in vitro, reducing A549 cell viability in co-culture with Jurkat cells[1].
ICD inducer-2 (48 h) exhibits broad-spectrum antiproliferative activity across multiple cancer cell lines with IC50 values from 8 ± 3 nM (MCF-7) to 47 ± 12 nM (A549/TxR), and overcomes paclitaxel resistance in A549/TxR cells with an RI of 4.7[1].
ICD inducer-2 (5-20 nM; 48 h) induces dose-dependent G2/M phase arrest in A549 cells, with corresponding arrest rates of 20.16%, 32.83%, and 40.30%, and modulates cell cycle regulatory proteins[1].
ICD inducer-2 (5-20 nM; 48 h) induces dose-dependent mitochondria-mediated apoptosis in A549 cells, increasing late-stage apoptosis and modulating apoptosis-related protein expression[1].
ICD inducer-2 (5-20 nM; 24 h) inhibits A549 cell migration in a dose-dependent manner[1].
ICD inducer-2 (5-20 nM; 8 h) inhibits HUVEC tube formation in a dose-dependent manner[1].

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

ICD inducer-2 Related Antibodies

Western Blot Analysis[1]

Cell Line: A549 cells
Concentration: 0.2, 1, 5, 25 μM
Incubation Time: 2 h
Result: Effectively suppressed the formation of the EBI/β-tubulin complex band, confirming binding to the colchicine-binding site on tubulin.

Immunofluorescence[1]

Cell Line: A549 cells
Concentration: 10, 20 nM
Incubation Time: 48 h
Result: Induced obvious microtubule network depolymerization, characterized by disorganized structures and diminished fluorescence signal.
Induced more severe disruption than colchicine at 20 nM.

Cell Viability Assay[1]

Cell Line: A549 cells, Jurkat cells
Concentration: 8, 16, 32, 64 nM
Incubation Time: 12-24 h
Result: Significantly reduced the viability of A549 cells in the co-culture group compared to the A549 monoculture group in a dose-dependent manner, indicating immunostimulatory potential.

Cell Cycle Analysis[1]

Cell Line: A549 cells
Concentration: 5, 10, 20 nM
Incubation Time: 48 h
Result: Induced G2/M phase arrest with blocking rates of 20.16% (5 nM), 32.83% (10 nM), and 40.30% (20 nM) in a dose-dependent manner.
Regulated the expression of cell cycle proteins Cdc25c, CDK7, cyclin B1, and P21.

Apoptosis Analysis[1]

Cell Line: A549 cells
Concentration: 5, 10, 20 nM
Incubation Time: 48 h
Result: Significantly increased late-stage apoptosis in a dose-dependent manner.
Downregulated antiapoptotic protein Bcl-2, upregulated proapoptotic proteins Bax and Bim-1, and increased cleaved caspase 3, cleaved caspase 9, and cleaved PARP levels.
Parmacokinetics
Species Dose Route T1/2 Tmax Cmax AUC0-24 AUC0-∞ MRT0-∞ F
Rat[1] 25 mg/kg i.v. 2.14 ± 0.33 h 0.08 ± 0.00 h 35188.87 ± 7938.18 ng/mL 22694.09 ± 3190.36 ng·h/mL 23328.92 ± 3029.44 ng·h/mL 1.40 ± 0.19 h /
Rat[1] 25 mg/kg i.p. 1.71 ± 0.18 h 0.33 ± 0.14 h 5208.96 ± 96.58 ng/mL 14481.33 ± 1309.32 ng·h/mL 15062.86 ± 1271.55 ng·h/mL 2.53 ± 0.19 h 64.57 %
In Vivo

ICD inducer-2 (Compound 17) (5-15 mg/kg; i.v.; once every two days; 28 days) achieves dose-dependent tumor growth inhibition of up to 82.0% in a paclitaxel-resistant A549/TxR xenograft mice models with no evident major organ toxicity at the maximal tested dose[1].
ICD inducer-2 (10-15 mg/kg; i.v.; once every two days; 14 days) achieves dose-dependent tumor growth inhibition of up to 81.6% in a Lewis lung carcinoma xenograft mice models, while effectively activating antitumor immune responses via increased T cell infiltration and pro-inflammatory cytokine production, with a favorable safety profile at tested doses[1].

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

Animal Model: BALB/c-nu nude mice with A549/TxR xenograft (male)[1]
Dosage: 5 mg/kg; 10 mg/kg; 15 mg/kg
Administration: i.v.; once every two days; 28 days
Result: Achieved tumor growth inhibition rates of 67.3%, 77.1%, and 82.0% at doses of 5, 10, and 15 mg/kg, respectively.
Showed a tumor growth inhibition rate of 77.1% at 10 mg/kg, which was markedly greater than that of the same dose of Paclitaxel (HY-B0015) (17.6%).
Revealed no evident toxicity in major organs at the maximal dose of 15 mg/kg.
Animal Model: C57BL/6N mice with Lewis lung carcinoma xenograft[1]
Dosage: 10 mg/kg; 15 mg/kg
Administration: i.v.; once every two days; 14 days
Result: Achieved tumor growth inhibition rates of 72.4% at 10 mg/kg and 81.6% at 15 mg/kg.
Showed a tumor growth inhibition rate of 72.4% at 10 mg/kg, which surpassed that of the same dose of paclitaxel (64.2%).
Increased the proportions of CD4+ and CD8+ T cells in tumor tissue to 7.008% and 7.439% at 10 mg/kg, respectively, significantly higher than the blank control group (3.334% and 3.658%) and slightly greater than the Paclitaxel group (6.627% and 6.559%).
Increased the proportions of CD4+ and CD8+ T cells in tumor tissue to 9.239% and 8.604% at 15 mg/kg, respectively.
Significantly increased serum levels of IFN-γ, IL-2, and IL-12, with higher levels than paclitaxel at the 10 mg/kg dose.
Induced marked calreticulin exposure and HMGB1 release in tumor cells, with greater effects than paclitaxel at the 10 mg/kg dose.
Showed no significant changes in body weight and no obvious toxicity in major organ tissues at 15 mg/kg.
Molecular Weight

385.44

Formula

C22H15N3O2S
CAS No.
SMILES

N#CC1=C(NC2=CC(C3=CC=CS3)=CC=C2)C4=CC5=C(C=C4N=C1)OCCO5
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Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
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Keywords:

ICD inducer-23069681-35-9ICD inducer2ICD inducer 2Microtubule/TubulinApoptosisBcl-2 FamilyCaspasePARPpoly ADP ribose polymeraselung carcinomacolchicine binding siteCD4+ T cellsCD8+ T cellsxenograft modelsmicrotubule dynamicstubulinA549 cellsimmunogenic cell deathtumor microenvironmentInhibitorinhibitorinhibit

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