Carboetomidate
Carboetomidate is a pyrrole derivative analogous to the sedative-hypnotic drug Etomidate, which induces general anesthesia while avoiding the inhibition of adrenal steroid synthesis. Carboetomidate enhances GABAA receptor function via β2/β3 subunits, inhibits neuronal nicotinic acetylcholine receptors (nAChR) and 5-HT3A receptors, and increases plasma IL-10 levels during endotoxemia. Carboetomidate is applicable to research related to sepsis and sleep disorders.
Para uso exclusivo en investigación. No vendemos a pacientes.
- No. CAS: 1257067-10-9
- Fòrmula: C15H17NO2
- Peso molecular:243.31
-
Almacenamiento:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Actividad biológica
-
Chemical Information
- Pureza y Documentación
- Referencias
-
Help & FAQs
Ver todos los productos específicos de isoformas 5-HT Receptor
More
Actividad biológica
Descripciòn
|
IL-10 |
GABAA |
nAChR |
5-HT3A Receptor |
In Vitro
Carboetomidate potently inhibits human 5-HT3A receptor function in Tetracycline (HY-A0107)-induced HEK293-TetR cells, with an IC50 of 1.9 µM for integrated current inhibition; this action occurs via reducing peak current amplitude and accelerating receptor desensitization, with significant inhibition observed at its hypnotic concentration[3].
Carboetomidate accelerates the deactivation rate of human 5-HT3A receptors in excised outside-out patches from Tetracycline-induced HEK293-TetR cells[3].
Carboetomidate (10 μM; 90-second pre-perfusion, followed by 90-second co-perfusion with EC5-10 GABA) potentiates currents mediated by human wild-type α1β2γ2L GABAA receptors by 390%, but does not potentiate currents mediated by Etomidate-insensitive mutant α1β2(M286W)γ2L GABAA receptors[5].
Carboetomidate potently inhibits human α4β2 neuronal nicotinic acetylcholine receptors expressed in Xenopus laevis oocytes with an IC50 of 13 μM[6].
Carboetomidate (48 h) inhibits cortisol synthesis in human adrenocortical carcinoma H295R cells with an IC50 of 2.6 μM[5].
Carboetomidate (40 μM) produces minimal (2.1%) inhibition of human NR1B/NR2A NMDA receptors expressed in Xenopus laevis oocytes[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
Carboetomidate (14 mg/kg; i.v.; every 15 minutes; 8 total doses) does not alter plasma ACTH, corticosterone, TNF-α, IL-1β, or IL-6 responses to LPS-induced endotoxemia, but increases peak plasma IL-10 concentrations to 21 ng/mL in male Sprague-Dawley rats[2].
Carboetomidate (1-40 μM; immersion; continuous exposure during assessment) is a potent hypnotic in Xenopus laevis tadpoles with an LORR EC50 of 5.4 μM[5].
Carboetomidate (7-28 mg/kg; i.v.; bolus with saline flush) is a potent hypnotic in adult male Sprague-Dawley rats with an LORR ED50 of 7 mg/kg, a 33 sec onset time at 28 mg/kg, and a dose-dependent LORR duration with a slope of 16 min/(log mg/kg)[5].
Carboetomidate (14 mg/kg; i.v.; bolus with saline flush) at a hypnotic dose causes minimal hemodynamic changes in adult male Sprague-Dawley rats, with effects comparable to vehicle[5].
Carboetomidate (14 mg/kg; i.v.; bolus with saline flush) at a hypnotic dose does not suppress adrenocortical function in adult male Sprague-Dawley rats, as evidenced by ACTH1-24-stimulated serum corticosterone concentrations comparable to vehicle control[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:Sprague-Dawley (adult male, 320-370 gm, LPS-induced endotoxemia)[2]
-
Dosage:14 mg/kg
-
Administration:i.v.; single dose
-
Result:Showed no difference in plasma ACTH concentrations (peaked at 430 pg/mL 30-120 minutes post-LPS) compared to control values at any time point.
Showed no difference in plasma corticosterone concentrations (peaked at 480 ng/mL 120 minutes post-LPS) compared to control values at any time point.
Showed no difference in plasma concentrations of TNF-α, IL-1β, IL-6, and IL-10 (increased by at least 10-fold post-LPS) compared to control values at any time point.
-
Animal Model:Sprague-Dawley (adult male, 320-370 gm, LPS-induced endotoxemia)[2]
-
Dosage:14 mg/kg
-
Administration:i.v.; every 15 minutes; 8 total doses
-
Result:Showed no difference in plasma ACTH concentrations (peaked at 430 pg/mL 30-120 minutes post-LPS) compared to control values at any time point.
Showed no difference in plasma corticosterone concentrations (peaked at 410 ng/mL 120 minutes post-LPS) compared to control values at any time point.
Showed no difference in plasma TNF-α concentrations (increased by at least 10-fold post-LPS) compared to control values at any time point.
Showed no difference in peak plasma IL-1β concentration (210 pg/mL) compared to control values.
Showed no difference in peak plasma IL-6 concentration (52 ng/mL) compared to control values.
Increased peak plasma IL-10 concentration to 21 ng/mL, which was elevated relative to the control group's peak of 8 ng/mL.
-
Animal Model:Xenopus laevis tadpoles (early prelimb-bud stage)[5]
-
Dosage:1 μM; 10 μM; 40 μM
-
Administration:immersion; continuous exposure during assessment
-
Result:Induced loss of righting reflex (LORR) in all tadpoles at 10-40 μM.
Reversed LORR in all tadpoles when moved to fresh water.
Achieved an EC50 for LORR of 5.4 μM.
-
Animal Model:Sprague-Dawley rats (adult male, 300-500 gm)[5]
-
Dosage:7 mg/kg (ED50 dose); 28 mg/kg; additional discrete doses
-
Administration:i.v.; bolus with saline flush
-
Result:Achieved an ED50 for LORR of 7 mg/kg.
Induced LORR in all rats at highest doses with no obvious toxicity.
Produced an onset time for LORR of 33 sec at 28 mg/kg.
Increased duration of LORR approximately linearly with the logarithm of the dose, with a slope of 16 min/(log mg/kg).
-
Animal Model:Sprague-Dawley rats (adult male, 300-500 gm)[5]
-
Dosage:14 mg/kg
-
Administration:i.v.; bolus with saline flush
-
Result:Caused no significant difference in mean arterial blood pressure compared to DMSO vehicle alone during the study period.\nProduced ACTH1-24-stimulated serum corticosterone concentration of 330 ng/mL, which was not significantly different from vehicle control values.
Chemical Information
-
No. CAS 1257067-10-9
-
Peso molecular 243.31
-
Fòrmula C15H17NO2
-
SMILES
[C@H](C)(N1C(C(OCC)=O)=CC=C1)C2=CC=CC=C2
-
Envío
Room temperature in continental US; may vary elsewhere.
-
Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureza y Documentación
Referencias
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Carboetomidate Related Classifications
HY-121102 Related Classifications
Powered by Bioz