Carboxy-PTIO potassium
Modify Date: 2024-01-04 14:37:48
Carboxy-PTIO potassium structure
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Common Name | Carboxy-PTIO potassium | ||
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| CAS Number | 148819-94-7 | Molecular Weight | 315.386 | |
| Density | N/A | Boiling Point | 456.3ºC at 760 mmHg | |
| Molecular Formula | C14H17KN2O4 | Melting Point | 141-143°C | |
| MSDS | USA | Flash Point | 229.7ºC | |
Use of Carboxy-PTIO potassiumCarboxy-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]. |
| Name | Carboxy-PTIO, Potassium Salt |
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| Synonym | More Synonyms |
| 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]. |
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| Related Catalog | |
| 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 |
| 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 |
| 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 |
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Dietary supplementation with sodium nitrite can exert neuroprotective effects on global cerebral ischemia/reperfusion in mice.
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| 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 |