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Chemical Structure| 2645-32-1 Chemical Structure| 2645-32-1

Structure of PR-619
CAS No.: 2645-32-1

Chemical Structure| 2645-32-1

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CAS No.: 2645-32-1

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PR-619 is a broad-spectrum and reversible inhibitor of the deubiquitinylating enzymes (DUBs) with EC50 of 1-20 μM and it was developed for chemotherapy.

Synonyms: 2,6-Diamino-3,5-dithiocyanopyridine; DUB Inhibitor V

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Product Details of PR-619

CAS No. :2645-32-1
Formula : C7H5N5S2
M.W : 223.28
SMILES Code : NC1=NC(N)=C(SC#N)C=C1SC#N
Synonyms :
2,6-Diamino-3,5-dithiocyanopyridine; DUB Inhibitor V
MDL No. :MFCD00830384
InChI Key :ZXOBLNBVNROVLC-UHFFFAOYSA-N
Pubchem ID :2817763

Safety of PR-619

GHS Pictogram:
Signal Word:Warning
Hazard Statements:H317-H319
Precautionary Statements:P280-P305+P351+P338

Isoform Comparison

Biological Activity

Target

  • DUB

    Plpro, EC50:14.2 μM

  • UCH

    UCH-L3, EC50:2.95 μM

    UCH-L5, EC50:12.8 μM

  • USP/UBP

    USP5, EC50:4.90 μM

    USP28, EC50:6.24 μM

In Vitro:

Cell Line
Concentration Treated Time Description References
T24/R cells 10–45 μM 48 hours PR-619 significantly inhibited cell viability and induced apoptosis. PMC8584183
T24/R cells 20 μM 48 hours PR-619 induced G2/M phase cell cycle arrest and increased the expression of ER stress-related apoptosis markers. PMC8584183
Kyse30 2-20 μmol/L 48 hours PR-619 inhibited ESCC cell growth and induced G2/M cell cycle arrest by downregulating cyclin B1 and upregulating p21. Meanwhile, PR-619 led to the accumulation of ubiquitylated proteins, induced ER stress and triggered apoptosis by the ATF4-Noxa axis. Moreover, the ER stress increased cytoplasmic Ca2+ and then stimulated autophagy through Ca2+-CaMKK β-AMPK signalling pathway. PMC8571299
Kyse450 2-20 μmol/L 48 hours PR-619 inhibited ESCC cell growth and induced G2/M cell cycle arrest by downregulating cyclin B1 and upregulating p21. Meanwhile, PR-619 led to the accumulation of ubiquitylated proteins, induced ER stress and triggered apoptosis by the ATF4-Noxa axis. Moreover, the ER stress increased cytoplasmic Ca2+ and then stimulated autophagy through Ca2+-CaMKK β-AMPK signalling pathway. PMC8571299
EC1 2-20 μmol/L 48 hours PR-619 inhibited ESCC cell growth and induced G2/M cell cycle arrest by downregulating cyclin B1 and upregulating p21. Meanwhile, PR-619 led to the accumulation of ubiquitylated proteins, induced ER stress and triggered apoptosis by the ATF4-Noxa axis. Moreover, the ER stress increased cytoplasmic Ca2+ and then stimulated autophagy through Ca2+-CaMKK β-AMPK signalling pathway. PMC7791184
EC109 2-20 μmol/L 48 hours PR-619 inhibited ESCC cell growth and induced G2/M cell cycle arrest by downregulating cyclin B1 and upregulating p21. Meanwhile, PR-619 led to the accumulation of ubiquitylated proteins, induced ER stress and triggered apoptosis by the ATF4-Noxa axis. Moreover, the ER stress increased cytoplasmic Ca2+ and then stimulated autophagy through Ca2+-CaMKK β-AMPK signalling pathway. PMC7791184
non-small cell lung cancer cell line A549 10 μM 24 hours PR-619 significantly inhibited the proliferation of A549 cells but increased cell motility. PMC7252467
mesothelioma cell line H2373 10 μM 24 hours PR-619 significantly inhibited the proliferation and motility of H2373 cells. PMC7252467
mouse ES-cell-derived motor neurons 20 μM 4 hours To evaluate the inhibitory effect of PR-619 on BoNT/A-mediated SNAP-25 cleavage, results showed that PR-619 significantly inhibited SNAP-25 cleavage. PMC8503599
HEK293 cells 20 μM 3 hours To evaluate the effect of PR-619 on BoNT/A LC degradation, results showed that PR-619 significantly promoted the degradation of BoNT/A LC. PMC8503599
MRC-5 lung fibroblasts 8 μM 15 or 30 minutes Increased caspase-8 ubiquitination and sensitized normal fibroblasts to TRAIL-mediated apoptosis PMC4786729
WI-38 embryonic lung fibroblasts 8 μM 15 or 30 minutes Increased caspase-8 ubiquitination and sensitized normal fibroblasts to TRAIL-mediated apoptosis PMC4786729
T24 1.25, 2.5, 5, 10, 20 μM 24, 48, 72 h To evaluate the antiproliferative effect of PR-619 on bladder cancer cells, the results showed that PR-619 had antiproliferative activity against all analyzed cell lines, and the effect was both concentration- and time-dependent. PMC10045593
SV-HUC-1 1.25, 2.5, 5, 10, 20 μM 24, 48, 72 h To evaluate the antiproliferative effect of PR-619 on normal bladder epithelial cells, the results showed that PR-619 had antiproliferative activity against SV-HUC-1 cells, and the effect was both concentration- and time-dependent. PMC10045593
K9TCC-PU-NK 1.25, 2.5, 5, 10, 20 μM 24, 48, 72 h To evaluate the antiproliferative effect of PR-619 on canine bladder cancer cells, the results showed that PR-619 had antiproliferative activity against K9TCC-PU-NK cells, and the effect was both concentration- and time-dependent. PMC10045593
RDSVS-TCC1 1.25, 2.5, 5, 10, 20 μM 24, 48, 72 h To evaluate the antiproliferative effect of PR-619 on canine bladder cancer cells, the results showed that PR-619 had antiproliferative activity against RDSVS-TCC1 cells, and the effect was both concentration- and time-dependent. PMC10045593
oesophageal squamous cell carcinoma cells 20 μM PYR-41 reduced PR-619-induced apoptosis, G2/M cell cycle arrest, and autophagy, and alleviated ER stress by reducing the accumulation of poly-ubiquitinated proteins. PMC7791184

In Vivo:

Species
Animal Model
Administration Dosage Frequency Description References
Nude mice T24/R xenograft model Intraperitoneal 5 mg/kg Single injection, lasting 12 hours PR-619 enhanced the antitumor effect of cisplatin and significantly inhibited the growth of T24/R xenograft tumors. PMC8584183

Protocol

Bio Calculators
Preparing Stock Solutions 1mg 5mg 10mg

1 mM

5 mM

10 mM

4.48mL

0.90mL

0.45mL

22.39mL

4.48mL

2.24mL

44.79mL

8.96mL

4.48mL

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