Doxapram - CAS 309-29-5
Catalog number:
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Potassium Channel
Doxapram is a respiratory stimulant. Administered intravenously, doxapram stimulates an increase in tidal volume, and respiratory rate. Doxapram stimulates chemoreceptors in the carotid bodies of the carotid arteries, which in turn, stimulates the respiratory centre in the brain stem.
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Related CAS:
7081-53-0 (HCl)
White to off-white crystalline powder.
1-ethyl-4- (2-morpholin-4-ylethyl)- 3,3-diphenyl-pyrrolidin-2-one; AHR-619; AHR 619; AHR619; Doxapram; Doxapram hydrochloride, Brand name Dopram, Stimulex or Respiram
Soluble in DMSO, not in water
Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).
Shelf Life:
2 years if stored properly
Canonical SMILES:
1.Observational Study on Less Invasive Surfactant Administration (LISA) in Preterm Infants<29 Weeks - Short and Long-term Outcomes.
Teig N1, Weitkämper A1, Rothermel J1, Bigge N1, Lilienthal E1, Rossler L1, Hamelmann E1. Z Geburtshilfe Neonatol. 2015 Dec;219(6):266-273. Epub 2015 Nov 9.
Background: A recent trial has demonstrated short-term benefits of a new minimal invasive procedure of surfactant administration in spontaneously breathing preterm infants ≥26 weeks (less invasive surfactant administration, LISA). Aim: To assess safety as well as short- and long-term outcomes of the LISA procedure in preterm infants between 23-28 weeks of gestation. Study design: Preterm infants born between 23+0 and 28+6 weeks gestational age during 2 periods, 18 months before (Period 1, n=44) and 18 months after introduction of LISA (Period 2, n=53), were analyzed for neonatal outcomes. 52% of discharged infants were assessed for neurodevelopmental outcome at corrected age of 3 years. Results: In Period 2, 66% of the preterm infants needing surfactant were treated by the new method of LISA. In this period, fewer patient had to be ventilated during the first 3 days of life (42 vs. 77%, p<0.0005) and overall (55 vs. 77%, p=0.02). The median duration of mechanical ventilation was 2 vs.
2.Reversal of morphine-induced respiratory depression by doxapram in anesthetized rats.
Haji A1, Kimura S2, Ohi Y2. Eur J Pharmacol. 2016 Mar 30. pii: S0014-2999(16)30192-3. doi: 10.1016/j.ejphar.2016.03.053. [Epub ahead of print]
The present study was undertaken to investigate whether doxapram, a blocker of tandem pore K+ (TASK-1/-3) channels, is a useful tool for recovery from morphine-induced ventilatory disturbances. Spontaneous ventilation and the hind leg withdrawal response against noxious thermal stimulation were recorded simultaneously in anesthetized rats. Morphine (1.0mg/kg, i.v.) decreased the minute volume resulting from depression of the ventilatory rate and tracheal airflow. Concomitantly, it prolonged the latency of withdrawal response against the thermal stimulation. Subsequent intravenous injection of doxapram recovered the morphine-induced ventilatory depression. This effect of doxapram declined rapidly after a single injection (1.0-3.0mg/kg, i.v.) but persisted with a continuous infusion (0.33mg/kg/min). Neither single injection nor continuous infusion of doxapram had any detectable effect on the analgesic potency of morphine. The central respiratory activity was recorded from the phrenic nerve in anesthetized, vagotomized, paralyzed and artificially ventilated rats.
3.Breathing Stimulant Compounds Inhibit TASK-3 Potassium Channel Function Likely by Binding at a Common Site in the Channel Pore.
Chokshi RH1, Larsen AT1, Bhayana B1, Cotten JF2. Mol Pharmacol. 2015 Nov;88(5):926-34. doi: 10.1124/mol.115.100107. Epub 2015 Aug 12.
Compounds PKTHPP (1-{1-[6-(biphenyl-4-ylcarbonyl)-5,6,7,8-tetrahydropyrido[4,3-d]-pyrimidin-4-yl]piperidin-4-yl}propan-1-one), A1899 (2''-[(4-methoxybenzoylamino)methyl]biphenyl-2-carboxylic acid 2,4-difluorobenzylamide), and doxapram inhibit TASK-1 (KCNK3) and TASK-3 (KCNK9) tandem pore (K2P) potassium channel function and stimulate breathing. To better understand the molecular mechanism(s) of action of these drugs, we undertook studies to identify amino acid residues in the TASK-3 protein that mediate this inhibition. Guided by homology modeling and molecular docking, we hypothesized that PKTHPP and A1899 bind in the TASK-3 intracellular pore. To test our hypothesis, we mutated each residue in or near the predicted PKTHPP and A1899 binding site (residues 118-128 and 228-248), individually, to a negatively charged aspartate. We quantified each mutation's effect on TASK-3 potassium channel concentration response to PKTHPP. Studies were conducted on TASK-3 transiently expressed in Fischer rat thyroid epithelial monolayers; channel function was measured in an Ussing chamber.
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CAS 309-29-5 Doxapram

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