Bupivacaine hydrochloride monohydrate [73360-54-0]

Chemodex

Bupivacaine hydrochloride monohydrate [73360-54-0]

10

6.1

73360-54-0

Research Use Only

>98%

Danger,Excepted quantity

C18H28N2O . HCl . H2O

288.4. 36.5 . 18.0

Bupivacaine is an amino amide local anesthetic that decreases current amplitude and inhibits whole cell K+ currents in Ca2+-activated K+ channels and N-type voltage-gated (KCNA and KCNC) K+ channels. Bupivacaine also inhibits voltage-gated Na+ channels and tandem pore domain (TASK-2/KCNK-5) K+ channels. The compound is cytotoxic at high concentrations inducing apoptosis and/or necrosis by interference with the mitochondrial energy transduction. Shown to inhibit aerobic ATP synthesis by (i) uncoupling of the oxidative phosphorylation (OXPHOS) and (ii) inhibition of the complex I of the respiratory. Other mechanisms include inhibition of the carnitine-acylcarnitine translocase or activation of the mitochondrial permeability transition pore (MPTP). The analgesic effects of bupivicaine are thought to potentially be due to its binding to the prostaglandin E2 receptors, subtype EP1 (PGE2EP1), which inhibits the production of prostaglandins, thereby reducing fever, inflammation, and hyperalgesia. It is employed as cAMP production inhibitor, it acts as a surfactant molecule possessing both hydrophilic and lipophilic properties, adrenergic antagonist and cholinesterase inhibitor. - Chemical. CAS: 73360-54-0. Formula: C18H28N2O . HCl . H2O. MW: 288.4. 36.5 . 18.0. Synthetic. Bupivacaine is an amino amide local anesthetic that decreases current amplitude and inhibits whole cell K+ currents in Ca2+-activated K+ channels and N-type voltage-gated (KCNA and KCNC) K+ channels. Bupivacaine also inhibits voltage-gated Na+ channels and tandem pore domain (TASK-2/KCNK-5) K+ channels. The compound is cytotoxic at high concentrations inducing apoptosis and/or necrosis by interference with the mitochondrial energy transduction. Shown to inhibit aerobic ATP synthesis by (i) uncoupling of the oxidative phosphorylation (OXPHOS) and (ii) inhibition of the complex I of the respiratory. Other mechanisms include inhibition of the carnitine-acylcarnitine translocase or activation of the mitochondrial permeability transition pore (MPTP). The analgesic effects of bupivicaine are thought to potentially be due to its binding to the prostaglandin E2 receptors, subtype EP1 (PGE2EP1), which inhibits the production of prostaglandins, thereby reducing fever, inflammation, and hyperalgesia. It is employed as cAMP production inhibitor, it acts as a surfactant molecule possessing both hydrophilic and lipophilic properties, adrenergic antagonist and cholinesterase inhibitor.

CCCCN1CCCCC1C(NC2=C(C)C=CC=C2C)=O.Cl.O

RT

2811

12352200