2. Apoptosis
  3. Apoptosis MDM-2/p53 Caspase
  4. Anticancer agent 311

Anticancer agent 311 是一种凋亡 (apoptosis) 诱导剂和 p53 调节剂。Anticancer agent 311 可提升 p53 水平、激活 cleaved caspase-3、降低 p-Cdc25C 水平，并阻断 p-p44/42 MAPK 的磷酸化过程。Anticancer agent 311 可诱导 G2/M 期停滞、以浓度和时间依赖性方式抑制癌细胞活力，且对非癌细胞毒性较低。Anticancer agent 311 可在小鼠异种移植模型中抑制肿瘤生长和血管生成，且未检测到毒性。Anticancer agent 311 可用于肺癌的研究。

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Anticancer agent 311

Anticancer agent 311 Chemical Structure

CAS No. : 421579-95-5

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Anticancer agent 311 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 311 is an apoptosis inducer and p53 modulator. Anticancer agent 311 increases p53 levels, activates cleaved caspase-3, reduces p-Cdc25C levels, and disrupts p-p44/42 MAPK phosphorylation. Anticancer agent 311 induces G2/M phase arrest, inhibits cancer cell viability in a concentration- and time-dependent manner, and exhibits low toxicity to non-cancer cells. Anticancer agent 311 prevents tumor growth and angiogenesis in mouse xenograft models without detectable toxicity. Anticancer agent 311 can be used for the research of lung cancer[1].

IC50 & Target

Caspase-3

 

体外研究
(In Vitro)

Anticancer agent 311 (#2714) (48 小时) 能有效抑制小鼠 Lewis 肺癌 LL/2 细胞的活力，IC50 为 5.43 μM，抑制小鼠乳腺癌 4T1 细胞的活力，IC50 为 6.12 μM，同时对非癌性 NIH-3T3 和 HK-2 细胞的毒性极低 (IC50 >40 μM)[1]。
Anticancer agent 311 (4-20 μM；24-72 小时) 以时间和浓度依赖的方式抑制 LL/2 细胞活力[1]。
Anticancer agent 311 (5-20 μM；48 小时) 可诱导小鼠 Lewis 肺癌 LL/2 细胞发生 G2/M 期阻滞，20 μM 组有 77.7%的细胞停滞于 G2/M 期[1]。
Anticancer agent 311 (5-20 μM；48 小时) 可呈浓度依赖性诱导小鼠 Lewis 肺癌 LL/2 细胞发生凋亡，在 20 μM 作用 48 小时后凋亡率达 50.2%，并会破坏这些细胞的线粒体膜电位[1]。
Anticancer agent 311 (2.5-10 μM；24 小时) 在处理小鼠 Lewis 肺癌 LL/2 细胞 24 小时后，可下调 p-Cdc25C、p-p44/42 MAPK 和 p-Akt，同时上调 p53 和剪切型 caspase-3，这支持其诱导细胞发生 G2/M 期阻滞和 caspase 依赖的细胞凋亡[1]。

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

Anticancer agent 311 相关抗体:

Cell Viability Assay[1]

Cell Line: Lewis lung carcinoma LL/2 cells
Concentration: 4 μM; 8 μM; 12 μM; 16 μM; 20 μM;
Incubation Time: 24 h; 48 h; 72 h
Result: Inhibited LL/2 cell viability in a time- and concentration-dependent manner.

Cell Cycle Analysis[1]

Cell Line: Lewis lung carcinoma LL/2 cells
Concentration: 5 μM; 10 μM; 20 μM
Incubation Time: 48 h
Result: Increased the percentage of LL/2 cells in the G2/M phase to 77.7% at 20 μM, accompanied by decreases in the G0/G1 and S phases.

Apoptosis Analysis[1]

Cell Line: Lewis lung carcinoma LL/2 cells
Concentration: 5 μM, 10 μM, 20 μM
Incubation Time: 48 h
Result: Increased the apoptosis rate of LL/2 cells to 22.9% with 5 μM, 45.1% with 10 μM, and 50.2% with 20 μM after 48 h.
Caused a concentration-dependent decrease in Rho 123 fluorescence, indicating collapse of mitochondrial membrane potential (ΔΨm).

Western Blot Analysis[1]

Cell Line: Lewis lung carcinoma LL/2 cells
Concentration: 2.5 μM, 5 μM, 10 μM
Incubation Time: 24 h
Result: Downregulated the expression of phosphorylated Cdc25C (p-Cdc25C), phosphorylated p44/42 MAPK (p-p44/42 MAPK), and phosphorylated Akt (p-Akt) in a concentration-dependent manner.
Upregulated the expression of p53 and cleaved caspase-3 in a concentration-dependent manner.
体内研究
(In Vivo)

Anticancer agent 311 (#2714) (25-100 mg/kg；腹腔注射；每日一次；连续 14 天) 在健康 C57BL/6 小鼠中耐受性良好，每日给药剂量高达 100 mg/kg、连续给药 14 天仍未检测到毒性[1]。
Anticancer agent 311 (#2714) (25-100 mg/kg；腹腔注射；每日一次；持续 28 天) 在 C57BL/6 小鼠中展现出强效抗肺癌活性，在 100 mg/kg 剂量下肿瘤生长抑制率最高可达 58.1%，同时还能延长生存期、减少血管生成并诱导肿瘤细胞凋亡，且未检测到毒性[1]。

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

Animal Model: C57BL/6 (male and female, 18-22 g)[1]
Dosage: 25 mg/kg; 50 mg/kg; 100 mg/kg
Administration: i.p.; daily; 14 days
Result: Caused no mortality, adverse clinical signs, or obvious pathological damage in any treated group.
Showed no significant differences in hematological parameters (WBC, RBC, HGB, HCT, PLT) between treated groups and vehicle control.
Showed no significant differences in serum biochemical parameters (HDL, TG, CHOL, CREA, BUN, GLU, ALP, ALB, TP, AST, ALT) between treated groups and vehicle control.
Animal Model: C57BL/6 (female, 6-8 weeks old, 18-22 g, subcutaneous implantation of LL/2 murine Lewis lung carcinoma cells)[1]
Dosage: 25 mg/kg; 50 mg/kg; 100 mg/kg
Administration: i.p.; daily; 28 days
Result: Achieved 45.1% tumor growth inhibition at 50 mg/kg compared to vehicle control.
Achieved 58.1% tumor growth inhibition at 100 mg/kg compared to vehicle control.
Significantly increased mouse survival compared to vehicle control across all doses.
Reduced CD31 staining by 37.4% in tumor tissues compared to vehicle control.
Reduced CD105 staining by 15.2% in tumor tissues compared to vehicle control.
Increased apoptotic tumor cells 11-fold compared to vehicle control.
Caused no significant changes in body weight during treatment.
分子量

439.46

Formula

C23H18FNO5S
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

Anticancer agent 311 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:

Anticancer agent 311421579-95-5Anticancer agent311Anticancer agent-311ApoptosisMDM-2/p53Caspasemurine Lewis lung carcinoma LL/2 cellsmouse mammary carcinoma 4T1 cellsNIH-3T3 cellsHK-2 cellsp-Cdc25Cp-p44/42 MAPKp53G2/M phase arrestapoptosiscleaved caspase-3Inhibitorinhibitorinhibit

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