Carboxy-PTIO potassium

Names

[ Name ]:
Carboxy-PTIO potassium

[Synonym ]:
1H-Imidazol-1-yloxy, 2-(4-carboxyphenyl)-4,5-dihydro-4,4,5,5-tetramethyl-3-oxido-, potassium salt (1:1)
Potassium [2-(4-carboxylatophenyl)-4,4,5,5-tetramethyl-3-oxido-4,5-dihydro-1H-imidazol-1-yl]oxidanyl
2-(4-Carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt
Carboxy-PTIO potassium salt
MFCD00216153
CARBOXY-PTIO

Biological Activity

[Description]:

Carboxy-PTIO potassium is a potent nitric oxide (NO) inhibitor that can make a quick reaction with NO to produce NO2. Carboxy-PTIO can prevent hypotension and endotoxic shock through the direct scavenging action against NO in lipopolysaccharide-stimulated rat model[1][2][3].

[Related Catalog]:

Research Areas >> Cardiovascular Disease

Signaling Pathways >> Immunology/Inflammation >> NO Synthase

Research Areas >> Inflammation/Immunology

Research Areas >> Metabolic Disease

[In Vitro]

Carboxy-PTIO potassium (200 μM; 1 h prior to physalin A; 24 hours) significantly suppresses the stimulation of NO expression induced by physalin A treatment, but no change is observed in Carboxy-PTIO treatment alone[1]. Carboxy-PTIO potassium (200 μM; 1 h prior to physalin A; 24 hours) reduces physalin A-induced cleavage of procaspase-3 and PARP, down-regulated ICAD expression,diminishing DNA fragmentation in nuclei[1]. Carboxy-PTIO potassium (200 μM; 1 h prior to physalin A; 24 hours) shows no effect on iNOS expression. However, decreased-mTOR and p-mTOR levels induced by physalin A is reversed by Carboxy-PTIO with concomitant suppression of LC3 I to LC3 II conversions in A375-S2 cells [1]. Western Blot Analysis[1] Cell Line: A375-S2 cells Concentration: 200 μM Incubation Time: 1 h prior to physalin A; 24 hours Result: Diminished physalin A-induced procaspase-3 and PARP cleavage.

[In Vivo]

Carboxy-PTIO (intravenous injection; 0.056-1.70 mg/kg/min; infused for 1 hr beginning 90 min after the LPS injection 90 min) treatment improves the hypotension, renal dysfunction and survival rate in Lps-treated rats. But it does not affect each parameter in naomal rats[3]. Animal Model: SD rats[3] Dosage: 0.056-1.70 mg/kg/min Administration: Intravenous injection; 0.056-1.70 mg/kg/min; infused for 1 hr beginning 90 min after the LPS injection 90 min Result: Exhibited a potent therapeutic value in endotoxin shock through the direct scavenging action against NO.

[References]

[1]. Hao He, et al.Nitric oxide induces apoptosis and autophagy; autophagy down-regulates NO synthesis in physalin A-treated A375-S2 human melanoma cells.Food Chem Toxicol. 2014 Sep;71:128-35.

[2]. T Akaike, et al. Antagonistic action of imidazolineoxyl N-oxides against endothelium-derived relaxing factor/.NO through a radical reaction. Biochemistry. 1993 Jan 26;32(3):827-32.

[3]. M Yoshid, et al. Therapeutic effects of imidazolineoxyl N-oxide against endotoxin shock through its direct nitric oxide-scavenging activity. Biochem Biophys Res Commun. 1994 Jul 29;202(2):923-30.

Chemical & Physical Properties

[ Boiling Point ]:
456.3ºC at 760 mmHg

[ Melting Point ]:
141-143°C

[ Molecular Formula ]:
C₁₄H₁₇KN₂O₄

[ Molecular Weight ]:
315.386

[ Flash Point ]:
229.7ºC

[ Exact Mass ]:
315.074707

[ PSA ]:
69.29000

[ LogP ]:
1.75670

[ Storage condition ]:
2-8°C

[ Water Solubility ]:
H2O: >20 mg/mL

MSDS

Click to get detail MSDS

Safety Information

[ Personal Protective Equipment ]:
Eyeshields;Gloves;type N95 (US);type P1 (EN143) respirator filter

[ Safety Phrases ]:
S24/25

[ RIDADR ]:
NONH for all modes of transport

[ WGK Germany ]:
3

Articles

Molecules involve in the self-protection of neurons against glucose-oxygen-serum deprivation (GOSD)-induced cell damage.

Brain Res. Bull. 79 , 169-76, (2009)

Molecules involved in self-protection of neurons against glucose/oxygen/serum deprivation (GOSD) were investigated. Trypan blue dye exclusion assay, Western blotting, ELISA, cytokine antibody array an...

Dietary supplementation with sodium nitrite can exert neuroprotective effects on global cerebral ischemia/reperfusion in mice.

J. Anesth. 29 , 609-17, (2015)

Nitrite-derived NO protects against middle cerebral artery occlusion in mice. We developed a new mouse model of global cerebral ischemia and reperfusion (GCI/R) involving reversible occlusion of the m...

Antagonistic action of imidazolineoxyl N-oxides against endothelium-derived relaxing factor/.NO through a radical reaction.

Biochemistry 32 , 827, (1993)

A labile inorganic free radical, nitric oxide (.NO), is produced by nitric oxide synthase from the substrate L-arginine in various cells and tissues. It acts as an endothelium-derived relaxing factor ...