1. Cell Cycle/DNA Damage Autophagy
  2. Endonuclease Autophagy
  3. PNR-3-80

PNR-3-80 is an endonuclease G (ENDOG) inhibitor with an IC50 of 0.67 μM. As a non-competitive binder to the ENDOG-substrate complex, PNR-3-80 specifically inhibits the endonuclease activity of ENDOG. PNR-3-80 reduces cell death induced by Cisplatin (HY-17394) and Docetaxel (HY-B0011), and inhibits DNA damage and autophagy (autophagy) induced by Etoposide (HY-13629). PNR-3-80 can be used in studies related to cell injury.

For research use only. We do not sell to patients.

PNR-3-80

PNR-3-80 Chemical Structure

CAS No. : 1424353-63-8

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Based on 1 publication(s) in Google Scholar

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Description

PNR-3-80 is an endonuclease G (ENDOG) inhibitor with an IC50 of 0.67 μM. As a non-competitive binder to the ENDOG-substrate complex, PNR-3-80 specifically inhibits the endonuclease activity of ENDOG. PNR-3-80 reduces cell death induced by Cisplatin (HY-17394) and Docetaxel (HY-B0011), and inhibits DNA damage and autophagy (autophagy) induced by Etoposide (HY-13629). PNR-3-80 can be used in studies related to cell injury[1][2].

In Vitro

PNR-3-80 (50 μM; 24 h) inhibits endonuclease G (ENDOG)-dependent DNA damage and autophagy induction in human hepatocytes[1].
PNR-3-80 potently inhibits recombinant mouse EndoG in high-throughput luciferase reporter gene assays, with an IC50 of 0.67 μM[2].
PNR-3-80 (1 μM for 1 h against mouse EndoG; 1 mM for 1 h against human EndoG) protects plasmid DNA from degradation by EndoG in plasmid nicking assays[2].
PNR-3-80 (pre-incubated for 2 h followed by co-incubation with Cisplatin for 24 h at a concentration of 50 μM) significantly protects 22Rv1 human prostate cancer cells that endogenously express EndoG against Cisplatin-induced cell death[2].
PNR-3-80 (preincubated for 2 h followed by co-incubation with docetaxel for 24 h at a concentration of 50 μM) significantly protects human prostate adenocarcinoma PC3 cells overexpressing EndoG from Docetaxel (HY-B0011)-induced cell death and DNA fragmentation[2].

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

Cell Cytotoxicity Assay[2]

Cell Line: Human prostate carcinoma 22Rv1 cells
Concentration: 50 μM
Incubation Time: 2 h pre-incubation, followed by 24 h co-incubation with Cisplatin
Result: Significantly inhibited Cisplatin-induced LDH release, reducing Cisplatin-induced cell death compared to controls without inhibitor.

Cell Cytotoxicity Assay[2]

Cell Line: EndoG-overexpressing human prostate adenocarcinoma PC3 cells
Concentration: 50 μM
Incubation Time: 2 h pre-incubation, followed by 24 h co-incubation with Docetaxel
Result: Significantly inhibited Docetaxel-induced LDH release, reducing Docetaxel-induced cell death compared to controls without inhibitor.
Significantly decreased Docetaxel-induced DNA fragmentation as measured by TUNEL staining.
Molecular Weight

459.90

Formula

C24H14ClN3O3S

CAS No.
Appearance

Solid

Color

Light yellow to yellow

SMILES

O=C1NC(NC(/C1=C\C2=CN(C3=C2C=C(Cl)C=C3)C(C4=CC5=C(C=CC=C5)C=C4)=O)=O)=S

Shipping

Room temperature in continental US; may vary elsewhere.

Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
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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.

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PNR-3-80
Cat. No.:
HY-176835
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