2. Cell Cycle/DNA Damage Stem Cell/Wnt Apoptosis Epigenetics PI3K/Akt/mTOR
  3. Casein Kinase Survivin Epigenetic Reader Domain Akt Apoptosis Caspase MDM-2/p53
  4. CK2-TN03

CK2-TN03 是一种 ATP 竞争型的酪蛋白激酶 2 (CK2) 抑制剂，其 IC50 为 165 nM，Ki 为 20 nM。CK2-TN03 抑制 CK2 介导的 survivin 激活，并降低 CK2 依赖的 BRD4/MYCN 与 AKT1 磷酸化水平。CK2-TN03 通过抑制 survivin 发挥抗神经母细胞瘤作用，导致癌细胞有丝分裂灾难和凋亡 (apoptosis)。CK2-TN03 可用于神经母细胞瘤的相关研究。

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CK2-TN03

CK2-TN03 Chemical Structure

CAS No. : 313226-24-3

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CK2-TN03 相关抗体

Top Publications Citing Use of Products

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CK1 CK2

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Akt Akt1 Akt2 Akt3

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Caspase 1 Caspase 2 Caspase 3 Caspase 4 Caspase 5 Caspase 6 Caspase 7 Caspase 8 Caspase 9 Caspase 10 Caspase 12 Caspase Caspase 11 Caspase-13

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

CK2-TN03 is an ATP-competitive casein kinase 2 (CK2) inhibitor, with an IC50 of 165 nM and a Ki of 20 nM. CK2-TN03 inhibits CK2-mediated survivin activation and reduces CK2-dependent phosphorylation levels of BRD4/MYCN and AKT1. CK2-TN03 exerts anti-neuroblastoma effects by inhibiting survivin, leading to mitotic catastrophe and apoptosis of cancer cells. CK2-TN03 can be used in studies related to neuroblastoma[1].

IC50 & Target[1]

CK2

165 nM (IC50)

Caspase 3

 

Caspase-7

 

BRD4

 

Akt1

 

体外研究
(In Vitro)

CK2-TN03 (0.2-25.0 μM; 48 h) 可在髓母细胞瘤 DAOY 细胞株及多种神经母细胞瘤细胞株中诱导剂量依赖性细胞死亡，其 EC50 值范围为 0.31 至 1.95 μM；而在胶质母细胞瘤 U87 细胞中无活性 (EC50 >25 μM)[1]。
CK2-TN03 (0.35-1.0 μM; 48 h) 以时间依赖方式激活 CHP-212 神经母细胞瘤细胞中的 caspase 3/7，主要诱导 caspase 依赖性细胞凋亡[1]。
CK2-TN03 (0.5-1.0 μM; 24-48 h) 可诱导 CHP-212 神经母细胞瘤细胞发生 G2/M 期细胞周期阻滞及后续细胞死亡[1]。
CK2-TN03 (0.5 μM; 24 h) 可使 CHP-212 神经母细胞瘤细胞停滞于有丝分裂期，阻断细胞成功分裂并引发有丝分裂灾难与细胞死亡[1]。
CK2-TN03 (0.5 μM; 48 h) 可通过直接抑制 survivin 的 CK2 介导磷酸化，间接改变 AKT1/MDM2/p53 与 BRD4/MYCN 通路，下调 CHP-212 神经母细胞瘤细胞中 survivin 的活性与表达，同时不改变 CK2 的表达[1]。
CK2-TN03 (0.5 μM; 48 h) 不影响分化的静息态 SH-SY5Y 神经母细胞瘤细胞的活力，这类细胞的 survivin 表达水平较低[1]。
CK2-TN03 (1-10 μM; 72 h) 可在由 160 种癌细胞系组成的多样化细胞组中诱导细胞死亡，且具有显著的肿瘤实体选择性，对黑色素瘤、淋巴瘤、肺癌、神经母细胞瘤、卵巢癌、骨髓瘤、软组织癌和骨肉瘤细胞系的效力最高[1]。
CK2-TN03 (10 μM; 1 h) 在 MDCKII-MDR1 细胞中表现出极佳的通透性，外排作用可忽略不计，且不具备 P-gp 底物活性[1]。

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

CK2-TN03 相关抗体:

Apoptosis Analysis[1]

Cell Line: Neuroblastoma CHP-212
Concentration: 0.35, 0.5 and 1.0 μM
Incubation Time: 48 h (monitored every 2 h)
Result: Induced a time-dependent increase in caspase 3/7 activation, with significantly higher activation levels observed from 18 h onward compared to vehicle-treated controls.
Left a fraction of cell death unaffected by cotreatment with pan-caspase inhibitor Q-VD-OPh, while the inhibitor reduced most CK2-TN03-induced cell death.

Cell Cycle Analysis[1]

Cell Line: Neuroblastoma CHP-212
Concentration: 0.5 and 1.0 μM
Incubation Time: 24 h, 48 h
Result: Increased the percentage of cells in the G2/M phase and the subG1 (dead cell) population after 24 and 48 h of treatment, with significant increases observed at both concentrations and time points compared to controls.
Increased G2/M phase cells after 24 h at 0.5 μM and 1.0 μM.
Further elevated G2/M and subG1 populations after 48 h at both concentrations.

Cell Viability Assay[1]

Cell Line: Differentiated neuroblastoma SH-SY5Y
Concentration: 0.5 μM
Incubation Time: 48 h
Result: Did not reduce viability of differentiated SH-SY5Y cells, which had ~20% of the survivin protein levels present in undifferentiated cells.
体内研究
(In Vivo)

CK2-TN03 (40 mg/kg; i.p.; 每日一次共 28 天) 可显著抑制神经母细胞瘤异种移植瘤的生长并改善小鼠存活率，部分小鼠实现了肿瘤的长期控制或缓解[1]。

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

Animal Model: (Ncr)-Foxn1 nu nude mice (7-8 weeks old)[1]
Dosage: 40 mg/kg
Administration: i.p.; once daily; 28 days
Result: Reduced tumor growth rate, with tumor volume relative to baseline (VTx/VT0) reaching ~6 on day 28, compared to ~9 in vehicle controls.
Improved mouse survival: 5 treated mice survived to day 49, compared to 1 vehicle-treated mouse; 2 treated mice survived beyond day 85, with one showing complete tumor remission by day 14 and the other exhibiting a small, non-growing tumor mass post-treatment.
Increased p53 levels and decreased survivin levels and survivin phosphorylation in tumor tissue.
分子量

326.37

Formula

C17H14N2O3S
CAS 号
Sequence

Asp-Lys-Phe-Val-Gly-{Leu-methyl}-{Nle}-NH2
Sequence Shortening

DKFVG-{Leu-methyl}-{Nle}-NH2
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

CK2-TN03 相关分类

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Keywords:

CK2-TN03313226-24-3Casein KinaseSurvivinEpigenetic Reader DomainAktApoptosisCaspaseMDM-2/p53PKBProtein kinase BAKT1neuroblastoma cellsp53casein kinase 2survivinCK2αMDM2medulloblastoma DAOYBRD4MYCNInhibitorinhibitorinhibit

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