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.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Reinheit: 98.77%
- CAS. Nr.: 2649242-85-1
- Formel: C32H37ClIN5O4
- Molecular Weight:718.02
-
Speicherung:
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]
-
Biologische Aktivität
-
Chemical Information
- Reinheit & Dokumentation
- Verweise
-
Help & FAQs
Alle DNA/RNA Synthesis Isoform-spezifische Produkte anzeigen
More
Biologische Aktivität
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. Nr. 2649242-85-1
-
Appearance Solid
-
Molecular Weight 718.02
-
Formel 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
-
Versand
Room temperature in continental US; may vary elsewhere.
-
Speicherung
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)
Reinheit & Dokumentation
-
Data Sheet (279 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)
Verweise
[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]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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