2. Apoptosis
  3. Apoptosis
  4. DD-CIP2

DD-CIP2 是一种 DNA 损伤诱导剂。DD-CIP2 通过调节 DNA 损伤反应通路，引发强烈的 DNA 损伤、细胞周期阻滞和细胞凋亡 (apoptosis)。DD-CIP2 在体内以耐受性良好的剂量显示出显著的抗肿瘤疗效且无明显毒性。DD-CIP2 对一系列血液肿瘤和实体瘤来源的癌细胞系的卓越细胞毒性均不依赖于这些细胞的 BRCA1/2 状态。DD-CIP2 可用于小细胞肺癌 (SCLC) 和非小细胞肺癌 (NSCLC) 的研究。

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DD-CIP2

DD-CIP2 Chemical Structure

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DD-CIP2 相关抗体

Top Publications Citing Use of Products

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

DD-CIP2 is a DNA damage and apoptosis inducer. DD-CIP2 demonstrates effective anti-proliferative activity against multiple cancer cell. DD-CIP2 modulates the DNA damage response pathway, triggering robust DNA damage, cell cycle arrest, and apoptosis in vitro. DD-CIP2 demonstrates significant anti-tumor efficacy in vivo at well-tolerated doses, without substantial toxicity. DD-CIP2 exhibits superior cytotoxic potency against a broad panel of blood-and solid-tumor-derived cancer cell lines independent of their BRCA1/2 status. DD-CIP2 can be used for small-cell lung cancer (SCLC) and non small-cell lung cancer (NSCLC) research[1].

体外研究
(In Vitro)

DD-CIP2 能够靶向多种癌症，其对不同癌细胞系的 IC50 如下：Jurkat 细胞为 12 nM，KARPASS422 细胞为 12 nM，Raji 细胞为 11 nM，Daudi 细胞为 2 nM，TYK-nu 细胞为 9.3 nM，对 MDA-MB-436 细胞的 IC50 小于 10 nM，SU-DHL-5 细胞为 0.8 nM，MOLT-4 细胞为 4.6 nM [1]。
DD-CIP2 在 HEK293T 细胞中仅使 PARP1 占有率适度增加 (EC50 = 42 nM)[1]。
DD-CIP2 (0.1-100 nM，处理 24 小时) 在 HEK293T 细胞中诱导 PARP1-BRD4 相互作用，并在 GLC16 和 NCI-H82 细胞系中减少 DNA 损伤[1]。
DD-CIP2 (0.1-0.8 nM，处理 72 小时) 在 SU-DHL-5 细胞中证明了其对 PARP1-BRD4 结合的依赖性[1]。
DD-CIP2 (10 µM，处理 24 小时) 在 GLC16 细胞中阻滞细胞周期进程[1]。

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

DD-CIP2 相关抗体:

Western Blot Analysis[1]

Cell Line: HEK293T cells
Concentration: 0.1, 1, 10 and 100 nM
Incubation Time: 24 h
Result: Elevated levels of γH2AX and cleaved PARP1 in both GLC16 and NCI-H82 cell.
Increased the phosphorylation of RPA32 at Ser4/Ser8 in both GLC16 and NCI-H82 cell.

Cell Cycle Analysis[1]

Cell Line: GLC16 cells
Concentration: 10 μM
Incubation Time: 24 h
Result: Provoked a dose-dependent accumulation of 199 cells in the G2/M phase.
体内研究
(In Vivo)

DD-CIP2 (20 mg/kg，腹腔注射，单次给药连续 5 天或 28 天 ) 在人源小细胞肺癌异种移植小鼠模型中实现了强效且耐受性良好的抗肿瘤活性且无明显的全身毒性[1]。

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

Animal Model: GLC16 cells (2 × 106, s.c.) induced NU-Foxn1nu mice (8 weeks)[1]
Dosage: 20 mg/kg
Administration: i.p., once for 5 days
Result: Induced a dose-dependent increase in γH2AX and cleaved PARP1, confirming target engagement.
Was well tolerated at doses up to 20 mg/kg, with no significant body weight loss.
Animal Model: GLC16 cells (2 × 106, s.c.) induced NU-Foxn1nu mice (8 weeks)[1]
Dosage: 20 mg/kg
Administration: i.p., once for 28 days
Result: Showed strong tumor regression as early as day 3, with 210 durable suppression maintained throughout the experiment period.
Detected no obvious toxicity as indicated by steady body weight.
分子量

985.57

Formula

C52H54ClFN10O5S
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

DD-CIP2 相关分类

  • 摩尔计算器

  • 稀释计算器

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Help & FAQs
  • 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:

DD-CIP2ApoptosisDNA damageapoptosisanti-tumor efficacysmall-cell lung cancernon small-cell lung cancerInhibitorinhibitorinhibit

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