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

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.

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NERx 329

NERx 329 Chemical Structure

CAS No. : 2649242-85-1

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NERx 329 Related Antibodies

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Description

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].

In Vitro

NERx 329 (Compound 43) exhibits significantly enhanced relative cellular uptake in H460 non-small cell lung cancer cells[1].
NERx-329 (4.3-7.2 μM; 5 d) inhibits the proliferation of A549 non-small cell lung cancer cells in a dose-dependent manner, and its antiproliferative effect is enhanced when combined with Cisplatin (HY-17394)[2].
NERx-329 (30 μM; 2 h) slows the replication fork speed in A549 non-small cell lung cancer cells, but does not alter the replication fork speed in BRCA1-deficient triple-negative breast cancer cells MDA-MB-436[2].
NERx-329 (30 μM; 1 h) impairs replication fork restart in A549 non-small cell lung cancer cells and MDA-MB-436 BRCA1-deficient triple-negative breast cancer cells[2].
NERx-329 (2-5 μM; 7-10 d) inhibits the proliferation of BRCA1-deficient triple-negative breast cancer cell line MDA-MB-436. Combined use with Olaparib (HY-10162) induces cell death, and repeated administration maintains its antiproliferative activity[2].
NERx-329 (30 μM; 3 h) combined with Olaparib depletes RPA protection in MDA-MB-436 BRCA1-deficient triple-negative breast cancer cells, thereby triggering MRE11-dependent degradation of PARPi-induced single-stranded DNA (ssDNA) gaps[2].
NERx-329 (30 μM; 2 h) combined with Olaparib increases the formation of double-stranded DNA breaks in MDA-MB-436 BRCA1-deficient triple-negative breast cancer (TNBC) cells[2].
NERx-329 (5-10 μM; 3 d) combined with Olaparib induces extensive chromosome shattering in MDA-MB-436 BRCA1-deficient triple-negative breast cancer cells, increasing the proportion of shattered chromosomes to approximately 19%[2].
NERx-329 (2-3 μM; 5 days) combined with the PARP1-specific inhibitor Saruparib (HY-132167) induces cell death in MDA-MB-436 BRCA1-deficient triple-negative breast cancer cells, suppresses proliferation recovery of UWB1.289 BRCA1-deficient ovarian cancer cells, and enhances antiproliferative efficacy in BRCA1-complemented UWB1.289 ovarian cancer cells[2].
NERx-329 (3-6 μM; 48-120 h) induces dose-dependent G1-phase and S-G2-M-phase arrest as well as mitotic escape in MDA-MB-436 BRCA1-deficient triple-negative breast cancer cells and A549 non-small cell lung cancer cells, and no additional cell cycle effects occur when combined with PARP inhibitors[2].

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

NERx 329 Related Antibodies

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.
In Vivo

NERx 329 (25 mg/kg; i.p.; once daily) exhibits significant single-agent anticancer activity in BRCA1-deficient triple-negative breast cancer xenografts, and combination treatment with Olaparib completely abrogates tumor growth without increased toxicity[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Molecular Weight

718.02

Formula

C32H37ClIN5O4
CAS No.
SMILES

O=C(CCCC(N1N=C(CC1C2=C(Cl)N=C3C=C(OCC)C=CC3=C2)C4=CC=C(I)C=C4)=O)NCCCN5CCOCC5
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Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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NERx 329 Related Classifications

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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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