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.
For research use only. We do not sell to patients.
- CAS No.: 1257067-10-9
- Formula: C15H17NO2
- Molecular Weight:243.31
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
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Biological Activity
Description
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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. Further protocols information, click here.
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.
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Animal Model:Sprague-Dawley (adult male, 320-370 gm, LPS-induced endotoxemia)[2]
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Dosage:14 mg/kg
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Administration:i.v.; single dose
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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.
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Animal Model:Sprague-Dawley (adult male, 320-370 gm, LPS-induced endotoxemia)[2]
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Dosage:14 mg/kg
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Administration:i.v.; every 15 minutes; 8 total doses
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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.
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Animal Model:Xenopus laevis tadpoles (early prelimb-bud stage)[5]
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Dosage:1 μM; 10 μM; 40 μM
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Administration:immersion; continuous exposure during assessment
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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.
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Animal Model:Sprague-Dawley rats (adult male, 300-500 gm)[5]
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Dosage:7 mg/kg (ED50 dose); 28 mg/kg; additional discrete doses
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Administration:i.v.; bolus with saline flush
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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).
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Animal Model:Sprague-Dawley rats (adult male, 300-500 gm)[5]
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Dosage:14 mg/kg
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Administration:i.v.; bolus with saline flush
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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
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CAS No. 1257067-10-9
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Molecular Weight 243.31
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Formula C15H17NO2
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SMILES
[C@H](C)(N1C(C(OCC)=O)=CC=C1)C2=CC=CC=C2
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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LPS-Induced Endotoxemia/Systemic Inflammation
Lipopolysaccharide (LPS)-induced endotoxemia is a widely used in vivo model of acute systemic inflammation in which LPS, a Gram-negative bacterial endotoxin, activates innate immune signaling primarily through TLR4, leading to rapid and transient induction of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β in circulation and tissues. This cytokine surge is commonly used as a measurable readout of systemic inflammatory activation and immune dysregulation, and is typically assessed within hours after intraperitoneal LPS administration in mouse models of endotoxemia. The model captures key features of systemic inflammatory response syndrome, including cytokine release, immune cell activation, and downstream tissue responses, and has been used to evaluate anti-inflammatory interventions such as cytokine modulation, lipid mediators, and immune cell-targeting therapies.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Carboetomidate Related Classifications
HY-121102 Related Classifications
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