2. Cell Cycle/DNA Damage
  3. RAD51
  4. BRCA2-RAD51-IN-3

BRCA2-RAD51-IN-3 是一种 RAD51-BRCA2 蛋白互作抑制剂，其 EC50 为 29.35 μM，Kd 为 75.14 μM。BRCA2-RAD51-IN-3 可阻断 RAD51-BRCA2 的结合，损伤癌细胞中的同源重组，并诱导合成致死效应。BRCA2-RAD51-IN-3 对人胰腺癌细胞起作用，且在正常胰腺细胞中无活性。BRCA2-RAD51-IN-3 可用于胰腺癌的研究。

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BRCA2-RAD51-IN-3

BRCA2-RAD51-IN-3 Chemical Structure

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BRCA2-RAD51-IN-3 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

BRCA2-RAD51-IN-3 is a RAD51-BRCA2 protein-protein interaction inhibitor with an EC50 of 29.35 μM and a Kd of 75.14 μM. BRCA2-RAD51-IN-3 blocks RAD51-BRCA2 binding, impairs homologous recombination in cancer cells, and induces synthetic lethality. BRCA2-RAD51-IN-3 acts in human pancreatic cancer cells and shows no activity in normal pancreatic cells. BRCA2-RAD51-IN-3 can be used for the research of pancreatic cancer[1].

体外研究
(In Vitro)

BRCA2-RAD51-IN-3 (compound 19) 可在体外 ELISA 实验中抑制 RAD51-BRCA2 蛋白-蛋白相互作用，其 EC50 为 29.35 μM，最大抑制率为 76%[1]。
BRCA2-RAD51-IN-3 可直接与重组人源 RAD51 结合，通过 MST[1] 检测其 Kd 为 75.14 μM[1]。
BRCA2-RAD51-IN-3 (50 μM; 1 μM RAD51 plus 2-5 μM BRC4 peptide) 可结合至 RAD51-BRCA2 相互作用界面，这一点已通过 NMR 位移实验得到证实[1]。
BRCA2-RAD51-IN-3 (10-80 μM) 可剂量依赖性地抑制 BxPC-3 细胞中的同源重组，其 IC50 为 21.74 μM，在 80 μM 时抑制率达 81%[1]。
BRCA2-RAD51-IN-3 (10-60 μM) 可抑制 HEK-293 细胞中的同源重组，在 40 μM 时会减少 HR-proficient 细胞[1]。
BRCA2-RAD51-IN-3 可在 Cisplatin (HY-17394) 诱导的 DNA 损伤后破坏 BxPC-3 细胞中的 RAD51 灶形成，这与对 RAD51-BRCA2 介导的 DNA 修复的抑制作用一致[1]。
BRCA2-RAD51-IN-3 (40 μM; 6 days, in combination with 10 μM Olaparib (HY-10162) ) 可在 2D 培养的 BxPC-3 和 HPAC 细胞中协同降低细胞活力 (Interaction Index = 0.77 和 0.72)，对正常 H-6037 胰腺上皮细胞的活力无显著影响，并且可诱导 BxPC-3 和 HPAC 细胞发生凋亡，这一点可通过显著升高的 BAX/BCL2 比值得到证明。
BRCA2-RAD51-IN-3 (40-60 μM; 144 hours, in combination with 10 μM Olaparib) 可与 Olaparib 协同作用，降低 BxPC-3 3D 球状体的细胞活力、抑制其生长并诱导细胞死亡；处理 144 小时后，其 3D 相互作用指数为 0.85[1]。

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

BRCA2-RAD51-IN-3 相关抗体:

Cell Viability Assay[1]

Cell Line: BxPC-3 human pancreatic adenocarcinoma cells (2D culture)
Concentration: 40 μM (in combination with 10 μM olaparib)
Incubation Time: 6 days
Result: Had no significant effect on cell viability; in combination with olaparib, significantly enhanced antiproliferative activity with an Interaction Index of 0.77, indicating synergism.

Cell Viability Assay[1]

Cell Line: HPAC human pancreatic adenocarcinoma cells (2D culture)
Concentration: 40 μM (in combination with 10 μM olaparib)
Incubation Time: 6 days
Result: Had no significant effect on cell viability; in combination with olaparib, significantly enhanced antiproliferative activity with an Interaction Index of 0.72, indicating synergism.

Cell Viability Assay[1]

Cell Line: H-6037 normal human pancreatic epithelial cells (2D culture)
Concentration: 40 μM (in combination with 10 μM olaparib)
Incubation Time: 6 days
Result: The combination had no significant effect on cell viability.

Cell Viability Assay[1]

Cell Line: BxPC-3 human pancreatic adenocarcinoma cells (3D spheroid culture)
Concentration: 40-60 μM (in combination with 10 μM olaparib)
Incubation Time: 6 days
Result: Had no significant effect on spheroid viability or volume; in combination with olaparib, 60 μM significantly reduced spheroid viability and volume, and increased cell death, with a 3D Interaction Index of 0.85, indicating synergism.

Apoptosis Analysis[1]

Cell Line: BxPC-3 and HPAC human pancreatic adenocarcinoma cells
Concentration: 40 μM (in combination with 10 μM olaparib)
Incubation Time: 6 days
Result: Significantly increased the BAX/BCL2 ratio in both cell lines, indicating induction of apoptotic cell death.
分子量

367.33

Formula

C21H14NNaO4
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

BRCA2-RAD51-IN-3 相关分类

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  • Do most proteins show cross-species activity?

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Keywords:

BRCA2-RAD51-IN-3RAD51RAD51-BRCA2 protein-protein interactionhomologous recombinationhuman pancreatic cancer cellsnormal pancreatic cellsHEK-293 cellsHPAC cellsBxPC-3 cellssynthetic lethalitypancreatic cancerInhibitorinhibitorinhibit

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