2. Cell Cycle/DNA Damage
  3. DNA/RNA Synthesis
  4. NERx 329

NERx 329 是一种复制蛋白 A (RPA) 抑制剂，其 IC50 为 4.9 μM。NERx 329 阻断 RPA 与单链 DNA 的相互作用，可诱导功能性 RPA 耗竭、单链 DNA 缺口保护丧失、染色体碎裂及细胞死亡。NERx 329 可抑制 DNA 损伤应答信号通路，具有广泛的单药抗癌活性，能增强 DNA 损伤剂的活性。NERx 329 可用于 brca1 缺陷型乳腺癌、非小细胞肺癌、brca1 缺陷型卵巢癌的相关研究。

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NERx 329

NERx 329 Chemical Structure

CAS No. : 2649242-85-1

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NERx 329 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

NERx 329 is a replication protein A (RPA) inhibitor with an IC50 of 4.9 μM. NERx 329 blocks the interaction between RPA and single-stranded DNA, and induces functional RPA depletion, loss of single-stranded DNA gap protection, chromosome fragmentation and cell death. NERx 329 inhibits the DNA damage response signaling pathway, exhibits broad single-agent anticancer activity, and enhances the activity of DNA-damaging agents. NERx 329 can be used in research related to brca1-deficient breast cancer, non-small cell lung cancer, and brca1-deficient ovarian cancer[1][2].

体外研究
(In Vitro)

NERx 329 (Compound 43) 具有显著提升的 H460 非小细胞肺癌细胞中的相对细胞摄取量[1]。
NERx-329 (4.3-7.2 μM; 5 d) 可剂量依赖性地抑制 A549 非小细胞肺癌细胞的增殖，且与 Cisplatin (HY-17394) 联用可增强该抗增殖作用[2]。
NERx-329 (30 μM; 2 h) 可减慢 A549 非小细胞肺癌细胞中复制叉的速度，但不会改变 BRCA1 缺陷型三阴性乳腺癌细胞 MDA-MB-436 中的复制叉速度[2]。
NERx-329 (30 μM; 1 h) 会损伤 A549 非小细胞肺癌细胞和 MDA-MB-436 BRCA1 缺陷型三阴性乳腺癌细胞中的复制叉重启[2]。
NERx-329 (2-5 μM; 7-10 d) 可抑制 BRCA1 缺陷型三阴性乳腺癌细胞 MDA-MB-436 的增殖，与 Olaparib (HY-10162) 联合使用可诱导细胞死亡，且重复给药能维持其抗增殖活性[2]。
NERx-329 (30 μM; 3 h) 与 Olaparib 联合作用时，会耗尽 MDA-MB-436 BRCA1 缺陷型三阴性乳腺癌细胞中的 RPA 保护，进而导致 PARPi 诱导的单链 DNA (ssDNA) 缺口发生 MRE11 依赖性降解[2]。
NERx-329 (30 μM; 2 h) 联合 Olaparib 可增加 MDA-MB-436 BRCA1 缺陷型三阴性乳腺癌 (TNBC) 细胞中双链 DNA 断裂的形成[2]。
NERx-329 (5-10 μM; 3 d) 与 Olaparib 联用可在 MDA-MB-436 BRCA1 缺陷型三阴性乳腺癌细胞中诱导广泛的染色体碎裂，将碎裂染色体的比例提升至约 19%[2]。
NERx-329 (2-3 μM; 5 days) 与 PARP1 特异性抑制剂 Saruparib (HY-132167) 联用可诱导 MDA-MB-436 BRCA1 缺陷型三阴性乳腺癌细胞死亡，抑制 UWB1.289 BRCA1 缺陷型卵巢癌细胞的增殖恢复，并增强 BRCA1 补全型 UWB1.289 卵巢癌细胞的抗增殖效力[2]。
NERx-329 (3-6 μM; 48-120 h) 可在 MDA-MB-436 BRCA1 缺陷型三阴性乳腺癌细胞和 A549 非小细胞肺癌细胞中诱导剂量依赖性的 G1 期和 S-G2-M 期阻滞以及有丝分裂逃逸，与 PARP 抑制剂联用时无额外的细胞周期效应[2]。

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

NERx 329 相关抗体:

Cell Proliferation Assay[2]

Cell Line: A549 non-small cell lung cancer (NSCLC) cells
Concentration: 4.3 μM; 7.2 μM; 4.3 μM combined with 10 μM Cisplatin
Incubation Time: 5 days
Result: Caused a dose-dependent decrease in cellular proliferation.
Reduced proliferation to a level comparable to treatment with 7.2 μM NERx-329 alone when combined with 10 μM cisplatin.

Cell Proliferation Assay[2]

Cell Line: MDA-MB-436 BRCA1-deficient TNBC cells
Concentration: 2 μM; 2 μM combined with 1 μM Olaparib; 2.5 μM initial dose with 5 μM second dose; 5 μM initial dose with 5 μM second dose
Incubation Time: 7 days; 10 days
Result: Inhibited proliferation within 24 h as a single agent, with confluence stabilizing for 4 days before increasing; blocked this recovery and reduced confluence when administered as a second dose.
Resulted in no measurable growth and a reduction in confluence over 7 days when combined with olaparib, indicative of cell death.

Cell Proliferation Assay[2]

Cell Line: MDA-MB-436 BRCA1-deficient TNBC cells, UWB1.289 BRCA1-deficient ovarian cancer cells, BRCA1-complemented UWB1.289 ovarian cancer cells
Concentration: 3 μM; 3 μM combined with 3 nM Saruparib (MDA-MB-436); 2 μM; 2 μM combined with 50 nM Saruparib (UWB1.289); 2 μM; 2 μM combined with 25 μM Saruparib (BRCA1-complemented UWB1.289)
Incubation Time: 5 days
Result: Resulted in no measurable growth and increased Cytotox Red uptake indicative of cell death when combined with saruparib in MDA-MB-436 cells.
Prevented proliferation recovery seen with single-agent NERx-329 when combined with saruparib in UWB1.289 cells.
Produced greater antiproliferative efficacy than either single agent when combined with saruparib in BRCA1-complemented UWB1.289 cells.

Cell Cycle Analysis[2]

Cell Line: MDA-MB-436 BRCA1-deficient TNBC cells, A549 NSCLC cells
Concentration: 3 μM; 3 μM combined with 1 μM Olaparib (flow cytometry); 3 μM; 6 μM; 3 μM combined with 3 nM Saruparib; 6 μM combined with 3 nM Saruparib (FUCCI assays)
Incubation Time: 48 h (flow cytometry); up to 120 h (FUCCI assays)
Result: Showed minimal cell cycle changes as a single agent in flow cytometry; left changes driven by olaparib alone unaltered when combined with olaparib.
Induced a biphasic cell cycle effect in FUCCI assays: initial modest increase in S-G2-M phase, followed by large accumulation in G1 phase, with dose-dependent delays in G1, G1/S, and S-G2-M phases, and increased mitotic bypass; triggered similar G1 accumulation in A549 FUCCI cells.
体内研究
(In Vivo)

NERx 329 (25 mg/kg；腹腔注射；每日 1 次) 在 BRCA1 缺陷型三阴性乳腺癌异种移植物中表现出显著的单药抗癌活性，与 Olaparib 联合用药可完全抑制肿瘤生长且未增加毒性[2]。

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

718.02

Formula

C32H37ClIN5O4
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

NERx 329 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:

NERx 3292649242-85-1NERx329NERx-329DNA/RNA SynthesisRPA70 domains AReplication Protein ARPA70 domains Bbrca1-deficient ovarian cancerH460 NSCLC cellsUWB1.289 BRCA1-deficient ovarian cancer cellsbrca1-deficient breast cancerA549 NSCLC cellsMDA-MB-436 BRCA1-deficient TNBC cellsnon-small cell lung cancerInhibitorinhibitorinhibit

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