2. Cell Cycle/DNA Damage Apoptosis Autophagy NF-κB Metabolic Enzyme/Protease Immunology/Inflammation
  3. PERK Apoptosis Autophagy Reactive Oxygen Species (ROS) Caspase Bcl-2 Family
  4. Anticancer agent 296

Anticancer agent 296 是一种抗癌剂，可激活 PERK-eIF2α-CHOP 信号通路以诱导内质网应激，进而调节 caspase 和 Bcl-2 家族蛋白，最终导致细胞凋亡 (apoptosis)。Anticancer agent 296 可增加活性氧 (ROS) 含量、降低线粒体膜电位并促进 Ca2+ 释放。Anticancer agent 296 可抑制细胞集落形成与 S 期细胞增殖，并诱导细胞自噬 (autophagy)。Anticancer agent 296 可用于非小细胞肺癌 (NSCLC) 的研究。

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Anticancer agent 296

Anticancer agent 296 Chemical Structure

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Anticancer agent 296 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

Anticancer agent 296 is a potent anticancer agent that activates the PERK-eIF2α-CHOP signaling pathway to induce endoplasmic reticulum stress, thereby regulating caspase and Bcl-2 family proteins, ultimately leading to apoptosis. Anticancer agent 296 increases intracellular levels of reactive oxygen species (ROS), reduces mitochondrial membrane potential, and promotes Ca2+ release. Anticancer agent 296 suppresses cell colony formation and S-phase cell proliferation, and induces autophagy. Anticancer agent 296 is applicable for research on non-small cell lung cancer (NSCLC)[1].

体外研究
(In Vitro)

Anticancer agent 296 (Compound 5b) (1.25-10 μM；作用 48 小时) 可强效抑制 A549 和 HeLa 癌细胞的增殖，对两种细胞的 IC50 值分别为 3.88 μM 和 3.89 μM，且对正常细胞具有良好的安全性[1]。
Anticancer agent 296 (1.94-3.88 μM；作用 48 h；经 Mitomycin C (HY-13316) 预处理 24 h) 可有效以浓度依赖方式抑制 A549 细胞的迁移，其中 3.88 μM 剂量可将伤口愈合率降至 8.19%[1]。
Anticancer agent 296 (1.94-7.76 μM；作用 24 h) 可下调 A549 细胞中 FAK 蛋白的表达，从而抑制细胞迁移；还可通过调控关键蛋白，激活 A549 细胞中的 PERK-eIF2α-CHOP 内质网应激通路及内源性凋亡通路[1]。
Anticancer agent 296 (1.94-7.76 μM；作用 7 天) 在浓度≥3.88 μM 时可有效抑制 A549 细胞的集落形成[1]。
Anticancer agent 296 (1.94-7.76 μM；作用 24 小时) 可通过上调 Beclin-1 并促进 LC3 I/II 转化来激活 A549 细胞中的自噬[1]。
Anticancer agent 296 (1.94-7.76 μM；作用 24 小时) 可呈剂量依赖性地诱导 A549 细胞发生 S 期阻滞，其中 7.76 μM 剂量可通过下调细胞周期相关蛋白将 S 期占比提升至 31.33%[1]。
Anticancer agent 296 (1.94-7.76 μM；作用 24 小时) 可呈浓度依赖性降低 A549 细胞的线粒体膜电位[1]。
Anticancer agent 296 (1.94-7.76 μM；作用 24 h) 可提升 A549 细胞内的 ROS 水平[1]。
Anticancer agent 296 (3.88-7.76 μM；作用 24 h) 可通过降低 GSH 水平并升高 MDA 水平在 A549 细胞中诱导氧化应激[1]。
Anticancer agent 296 (1.94-7.76 μM；作用 24 h) 可升高 A549 细胞内的钙离子浓度，其中 7.76 μM 浓度可诱导钙离子浓度升高 1.68 倍[1]。
Anticancer agent 296 (3.88 μM；24 h) 通过 PERK 通路诱导 A549 细胞产生内质网应激，这一点可被内质网空泡化现象证实[1]。
Anticancer agent 296 (1.94-7.76 μM；作用 24 小时) 可诱导 A549 细胞发生早期凋亡，其中 7.76 μM 浓度下早期凋亡率可升高至 11.14%[1]。

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

Anticancer agent 296 相关抗体:

Cell Proliferation Assay[1]

Cell Line: A549 (human lung adenocarcinoma), HeLa (human cervical cancer), NIH-3T3 (mouse embryonic fibroblast), THLE-2 (human immortalised liver)
Concentration: 1.25 μM, 2.5 μM, 5 μM and 10 μM
Incubation Time: 48 h
Result: Potently inhibited proliferation of A549 and HeLa cells with IC50 values of 3.88 μM and 3.89 μM, respectively.
Exhibited lower cytotoxicity against normal cells with IC50 values of 26.48 μM (NIH-3T3) and 12.08 μM (THLE-2).

Cell Migration Assay[1]

Cell Line: A549 cells
Concentration: 1.94 μM (0.5×IC₅₀), 3.88 μM (IC₅₀)
Incubation Time: 48 h; 24 h (with mitomycin c pre-treatment)
Result: Reduced scratch healing percentage from 29.31% (control) to 18.16% (1.94 μM) and 8.19% (3.88 μM) after 48 h. Inhibited migration even in the presence of Mitomycin c.

Western Blot Analysis[1]

Cell Line: A549 cells
Concentration: 1.94 μM (0.5×IC₅₀), 3.88 μM (IC₅₀), 7.76 μM (2×IC₅₀)
Incubation Time: 24 h
Result: Downregulated FAK protein expression compared to the control group.\nUpregulated p53, Bax, cleaved PARP, caspase-3, PERK, GRP78, p-eIF2α, CHOP, STIM1, and ORAI1; downregulated Bcl-2.

Cell Autophagy Assay[1]

Cell Line: A549 cells
Concentration: 1.94 μM (0.5×IC₅₀), 3.88 μM (IC₅₀), 7.76 μM (2×IC₅₀)
Incubation Time: 24 h
Result: Increased MDC fluorescence intensity (indicating enhanced autophagy) and upregulated Beclin-1 expression, while p62 decreased and LC3 I/II conversion was observed.

Cell Cycle Analysis[1]

Cell Line: A549 cells
Concentration: 1.94 μM (0.5×IC₅₀), 3.88 μM (IC₅₀), 7.76 μM (2×IC₅₀)
Incubation Time: 24 h
Result: Increased S phase percentage from 18.95% (control) to 24.72% (1.94 μM), 27.38% (3.88 μM), and 31.33% (7.76 μM). Reduced expression of Cyclin A2, Cyclin B1, and CDK2.

Apoptosis Analysis[1]

Cell Line: A549 cells
Concentration: 1.94 μM (0.5×IC₅₀), 3.88 μM (IC₅₀), 7.76 μM (2×IC₅₀)
Incubation Time: 24 h
Result: Increased early apoptosis rate from 2.48% (control) to 4.47% (1.94 μM), 9.34% (3.88 μM), and 11.14% (7.76 μM).
体内研究
(In Vivo)

Anticancer agent 296 (Compound 5b) (10-20 mg/kg；腹腔注射；每日给药；连续 12 天) 在 A549 异种移植瘤小鼠中表现出剂量依赖性的抗肿瘤功效，20 mg/kg 剂量组的肿瘤抑制率达 80.32%[1]。

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

Animal Model: BALB/c nu mice injected with A549 cells[1]
Dosage: 10 mg/kg; 20 mg/kg
Administration: i.p.; daily; 12 consecutive days
Result: Achieved tumor inhibition rates of 62.92% (10 mg/kg) and 80.32% (20 mg/kg). Induced DNA damage in tumor cells with γH2AX positive rates of 60.2% (10 mg/kg) and 69.3% (20 mg/kg). Inhibited tumor proliferation with Ki67 positive rates of 36.5% (10 mg/kg) and 24.4% (20 mg/kg). Observed no significant body weight changes or chronic organ damage.
分子量

519.43

Formula

C24H22BrF3N2OSi
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.
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参考文献

Anticancer agent 296 相关分类

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  • Do most proteins show cross-species activity?

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Keywords:

Anticancer agent 296Anticancer agent296Anticancer agent-296PERKApoptosisAutophagyReactive Oxygen Species (ROS)CaspaseBcl-2 FamilyProtein kinase R-like endoplasmic reticulum kinasePKR-like endoplasmic reticulum kinaseHeLaPERK-eIF2α-CHOP signaling pathwayapoptosisA549non-small cell lung cancerlung adenocarcinomareactive oxygen speciesmitochondrial membrane potentialendoplasmic reticulum stressInhibitorinhibitorinhibit

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