NERx 329
Based on 1 Customer Validation
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.
For research use only. We do not sell to patients.
- Purity: 98.77%
- CAS No.: 2649242-85-1
- Formula: C32H37ClIN5O4
- Molecular Weight:718.02
-
Storage:
4°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Biological Activity
-
Chemical Information
-
Solvent & Solubility
- Purity & Documentation
- References
-
Help & FAQs
All DNA/RNA Synthesis Isoforms
More
Biological Activity
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.
-
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 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 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 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.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
-
CAS No. 2649242-85-1
-
Appearance Solid
-
Molecular Weight 718.02
-
Formula C32H37ClIN5O4
-
Color Off-white to light yellow
-
SMILES
O=C(CCCC(N1N=C(CC1C2=C(Cl)N=C3C=C(OCC)C=CC3=C2)C4=CC=C(I)C=C4)=O)NCCCN5CCOCC5
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
4°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
Solvent & Solubility
DMSO : 5 mg/mL (6.96 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Purity & Documentation
-
Data Sheet (281 KB)
-
SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
-
Handling Instructions (2659 KB)
References
[1]. Gavande NS, et al. Structure-Guided Optimization of Replication Protein A (RPA)-DNA Interaction Inhibitors. ACS Med Chem Lett. 2020;11(6):1118-1124. Published 2020 Jan 2. [Content Brief]
[2]. VanderVere-Carozza PS, et al. Replication protein A protects lagging strand gaps, restricting PARP inhibitor-induced synthetic lethality in BRCA1-deficient tumors. Nucleic Acids Res. 2026;54(8):gkag396. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 1.3927 mL | 6.9636 mL | 13.9272 mL | 34.8180 mL |
| 5 mM | 0.2785 mL | 1.3927 mL | 2.7854 mL | 6.9636 mL |
NERx 329 Related Classifications
HY-171171 Related Classifications
Powered by Bioz
- NERx 329
- 2649242-85-1
- NERx329
- NERx-329
- DNA/RNA Synthesis
- RPA70 domains A
- Replication Protein A
- RPA70 domains B
- brca1-deficient ovarian cancer
- H460 NSCLC cells
- UWB1.289 BRCA1-deficient ovarian cancer cells
- brca1-deficient breast cancer
- A549 NSCLC cells
- MDA-MB-436 BRCA1-deficient TNBC cells
- non-small cell lung cancer
- Inhibitor
- inhibitor
- inhibit