2. Apoptosis Cell Cycle/DNA Damage
  3. Apoptosis Checkpoint Kinase (Chk) CDK DNA/RNA Synthesis Bcl-2 Family Caspase
  4. Apoptosis inducer 49

Apoptosis inducer 49 是一种选择性细胞毒性化合物，对 CCRF-CEM 白血病细胞具有高度特异性 (IC50 = 2.68 μM) 。Apoptosis inducer 49 可诱导 DNA 损伤 (γH2AX) 和复制应激，激活 Chk1-p21 通路，导致 S 期阻滞。Apoptosis inducer 49 通过线粒体途径 (抑制 Bcl-2 和激活 caspase-3) 诱导 CCRF-CEM 细胞凋亡 (apoptosis)。Apoptosis inducer 49 可用于白血病的研究。

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Apoptosis inducer 49

Apoptosis inducer 49 Chemical Structure

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Apoptosis inducer 49 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Apoptosis inducer 49 is a selective apoptosis inducer with high specificity against CCRF-CEM leukemia cells (IC50 = 2.68 μM). Apoptosis inducer 49 enhances RNA synthesis and replication stress, activates the Chk1-p21 axis, leading to S-phase arrest. Apoptosis inducer 49 can inhibit Bcl-2 and activate caspase-3. Apoptosis inducer 49 can be used for the study of Leukemia[1].

体外研究
(In Vitro)

Apoptosis inducer 49 (Compound 16j) 对 CCRF-CEM 细胞表现出强效的细胞毒性 (IC50 = 2.68 μM)，对其他癌细胞系和非癌细胞系无显著活性 (IC50 > 50 μM)，治疗指数 (TI) 为 18.66[1]。
Apoptosis inducer 49 (2.68-13.4 μM，24 小时) 可剂量依赖性地增加 CCRF-CEM 细胞的凋亡比例，并诱导显著的 S 期阻滞。在 2.68 μM 浓度下，早期凋亡 (Annexin V+/PI-) 细胞显著增加，同时 S 期细胞数量增加，G1 期和 G2/M 期细胞数量减少；而在 13.4 μM 浓度下，晚期凋亡 (Annexin V+/PI+) 细胞进一步积累，S 期阻滞效应更加显著[1]。
Apoptosis inducer 49 (2.68-13.4 μM，24 小时) 在 CCRF-CEM 细胞中表现出剂量依赖性的 DNA 复制抑制作用 (在 13.4 μM 时几乎完全抑制)，但 RNA 合成增强[1]。
Apoptosis inducer 49 (2.68-13.4 μM，24 小时) 使 CCRF-CEM 细胞中的细胞群向 P3 区 (高红/绿荧光) 转移，表明线粒体发生超极化 (ΔΨm 增加)，而非典型的坏死相关去极化[1]。
Apoptosis inducer 49 (2.68-13.4 μM，24 小时) 可诱导 DNA 损伤和复制压力，激活 Chk1-p21 轴导致 S 期阻滞，并通过线粒体途径 (Bcl-2 抑制和 caspase-3 激活) 触发 CCRF-CEM 细胞的凋亡[1]。

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

Apoptosis inducer 49 相关抗体:

Apoptosis Analysis[1]

Cell Line: CCRF-CEM cells
Concentration: 2.68 μM, 13.4 μM
Incubation Time: 24 h
Result: At 2.68 μM, early apoptotic (annexin V+/PI-) cells significantly increased.
At 13.4 μM, late apoptotic (annexin V+/PI+) cells further accumulated.
PI single-positive cells (necrosis markers) were extremely rare.

Western Blot Analysis[1]

Cell Line: CCRF-CEM cells
Concentration: 2.68 μM, 13.4 μM
Incubation Time: 24 h
Result: Caused a moderate increase in Cyclin A expression at both concentrations.
Total Chk1 levels remained stable or slightly elevated at 2.68 μM, while phospho-Chk1 (Ser345), a canonical marker of ATR-mediated replication checkpoint activation, was robustly induced at both 2.68 μM and 13.4 μM.
P21 expression was strongly induced at 2.68 μM.
Induced γH2AX at both concentrations.
Bcl-2 expression was diminished at 13.4 μM.
Caspase-3 was clearly diminished at high concentrations.

Cell Cycle Analysis[1]

Cell Line: CCRF-CEM cells
Concentration: 2.68 μM, 13.4 μM
Incubation Time: 24 h
Result: Caused significant S-phase arrest, at 2.68 μM, the proportion of cells in S phase increased, and the G1 and G2/M populations decreased; the effect was more pronounced at 13.4 μM.
分子量

575.82

Formula

C36H53N3O3
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

Apoptosis inducer 49 相关分类

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Keywords:

Apoptosis inducer 49Apoptosis inducer49Apoptosis inducer-49ApoptosisCheckpoint Kinase (Chk)CDKDNA/RNA SynthesisBcl-2 FamilyCaspaseCyclin dependent kinaseLupane triterpenoidsSelective cytotoxicityCCRF-CEM cellsDNA damage responseInhibitorinhibitorinhibit

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