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

ICD inducer-2 是一种免疫原性细胞死亡诱导剂。ICD inducer-2 结合微管蛋白 (tubulin) 上的秋水仙碱结合位点，从而抑制微管蛋白聚合。ICD inducer-2 在多种癌细胞系中展现出广谱抗增殖活性。ICD inducer-2 抑制细胞迁移，引发 G2/M 期阻滞并诱导凋亡 (apoptosis)。ICD inducer-2 促进 CD4+ 和 CD8+ T 细胞浸润至肿瘤微环境。ICD inducer-2 下调抗凋亡蛋白 Bcl-2，上调促凋亡蛋白 Bax 和 Bim-1，并提高剪切型 caspase 3、剪切型 caspase 9 以及剪切型 PARP 的水平。ICD inducer-2 可克服异种移植模型中的紫杉醇耐药性，实现肿瘤生长抑制。ICD inducer-2 可用于癌症相关研究，例如肺癌。

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ICD inducer-2

ICD inducer-2 Chemical Structure

CAS No. : 3069681-35-9

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ICD inducer-2 相关抗体

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

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

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

 

体外研究
(In Vitro)

ICD inducer-2 (Compound 17) (1.25-5 μM; 60 min) 可呈剂量依赖性抑制纯化微管蛋白的聚合[1]。
ICD inducer-2 (0.2-25 μM; 2 h) 可与 A549 细胞中微管蛋白上的秋水仙碱结合位点结合[1]。
ICD inducer-2 (10-20 nM; 48 h) 可在 10 nM 和 20 nM 浓度下破坏 A549 细胞中的微管网络[1]。
ICD inducer-2 (20-80 nM; 12 h) 可在 20、40 和 80 nM 浓度下强效诱导 A549 细胞发生免疫原性细胞死亡 (ICD)[1]。
ICD inducer-2 (8-64 nM; 12-24 h) 具有体外免疫刺激潜力，在与 Jurkat 细胞共培养的体系中，可降低 A549 细胞的存活率[1]。
ICD inducer-2 (48 h) 对多种癌细胞系具有广谱抗增殖活性，其 IC50 值范围为 8 ± 3 nM (MCF-7) 至 47 ± 12 nM (A549/TxR)，并可逆转 A549/TxR 细胞的紫杉醇耐药性，RI 为 4.7[1]。
ICD inducer-2 (5-20 nM; 48 h) 可诱导 A549 细胞发生剂量依赖性 G2/M 期阻滞，对应的阻滞率分别为 20.16%、32.83% 和 40.30%，并可调控细胞周期调控蛋白[1]。
ICD inducer-2 (5-20 nM; 48 h) 可诱导 A549 细胞发生剂量依赖性的线粒体介导的细胞凋亡，增加晚期凋亡水平并调控凋亡相关蛋白的表达[1]。
ICD inducer-2 (5-20 nM; 24 h) 可以剂量依赖的方式抑制 A549 细胞迁移[1]。
ICD inducer-2 (5-20 nM; 8 h) 可剂量依赖性抑制 HUVEC 管形成[1]。

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

ICD inducer-2 相关抗体:

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.
药代动力学
(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 %
体内研究
(In Vivo)

ICD inducer-2 (Compound 17) (5-15 mg/kg；静脉注射；每两天一次；28 天) 在紫杉醇耐药的 A549/TxR 异种移植小鼠模型中实现了剂量依赖性的肿瘤生长抑制，最高抑制率可达 82.0%，且在测试的最大剂量下未观察到明显的主要器官毒性[1]。
ICD inducer-2 (10-15 mg/kg；静脉注射；每两天一次；14 天) 在 Lewis 肺癌异种移植小鼠模型中实现了最高达 81.6%的剂量依赖性肿瘤生长抑制，同时可通过增加 T 细胞浸润和促炎细胞因子产生有效激活抗肿瘤免疫反应，且在测试剂量下具有良好的安全性特征[1]。

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.
分子量

385.44

Formula

C22H15N3O2S
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

ICD inducer-2 相关分类

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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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