(±)-Epibatidine dihydrochloride hydrate

• Catalog No.: E1145
• M. F.: C11H17Cl3N2O
• M. W.: 299.62448
• Purity: ≥98% (HPLC)

SYNONYMS

• IUPAC name: (2R)-2-(6-chloropyridin-3-yl)-7-azabicyclo[2.2.1]heptane hydrate dihydrochloride
• IUPAC Traditional name: (2R)-2-(6-chloropyridin-3-yl)-7-azabicyclo[2.2.1]heptane hydrate dihydrochloride
• Synonyms: exo-(±)-2-(6-Chloro-3-pyridinyl)-7-azabicyclo[2.2.1]heptane dihydrochloride hydrate

DATABASE IDS

• PubChem SID: 24894390

PROPERTIES

• Empirical Formula (Hill Notation): C11H13ClN2 · 2HCl · xH2O
• Purity: ≥98% (HPLC)
• Apperance: off-white powder
• Solubility: DMSO: >4 mg/mL
• Solubility: methanol: soluble4 mg/mL
• GHS Signal Word: Danger
• GHS Hazard statements: H300-H310
• European Hazard Symbols: Highly toxic (T+)
• Personal Protective Equipment: Eyeshields, Faceshields, full-face particle respirator type N100 (US), Gloves, respirator cartridge type N100 (US), type P1 (EN143) respirator filter, type P3 (EN 143) respirator cartridges
• GHS Precautionary statements: P264-P280-P301 + P310-P302 + P350-P310
• RID/ADR: UN 2811 6.1/PG 1
• Risk Statements: 27/28
• Safety Statements: 28-36/37-45
• Hazard Class: 6.1
• UN Number: 2811
• Packing Group: 1
• German water hazard class: 3

DETAILS

Description (English)

Biochem/physiol Actions
The activity of epibatidine at neuronal and neuromuscular nicotinic acetylcholine receptors was compared with the activity of nicotine and suxamethonium. Activation of ganglionic nicotinic receptors by epibatidine was shown in the guinea-pig ileum (contraction mediated by the cholinergic neurons of the ileum) and in pithed and atropinized rats (rise in blood pressure). Epibatidine also activated nicotinic receptors at the peripheral terminals of afferent C-fibres (rabbit ear) and in the brain (antidiuresis in rats). The agonistic effects of epibatidine were followed by long-lasting receptor desensitization. No antinociceptive effect of epibatidine was seen in rats at a dose free of motor impairment. On muscle end plate nicotinic receptors of the rat diaphragm (not responding to depolarizing agents by contraction), epibatidine was equipotent with suxamethonium in causing neuromuscular inhibition. On an extraocular muscle of the rabbit (responding to depolarizing agents by contraction) epibatidine in vitro and in situ caused a contraction at a 100-fold lower dose than suxamethonium. The Straub tail reaction in mice to epibatidine could be attributed to the sustained stimulation of motor end plate receptors of the "slow contracting" type of muscle fibres by epibatidine. Epibatidine was the most potent agonist on all neuronal and neuromuscular nicotinic receptors examined.

Description (简体中文)

Biochem/physiol Actions
The activity of epibatidine at neuronal and neuromuscular nicotinic acetylcholine receptors was compared with the activity of nicotine and suxamethonium. Activation of ganglionic nicotinic receptors by epibatidine was shown in the guinea-pig ileum (contraction mediated by the cholinergic neurons of the ileum) and in pithed and atropinized rats (rise in blood pressure). Epibatidine also activated nicotinic receptors at the peripheral terminals of afferent C-fibres (rabbit ear) and in the brain (antidiuresis in rats). The agonistic effects of epibatidine were followed by long-lasting receptor desensitization. No antinociceptive effect of epibatidine was seen in rats at a dose free of motor impairment. On muscle end plate nicotinic receptors of the rat diaphragm (not responding to depolarizing agents by contraction), epibatidine was equipotent with suxamethonium in causing neuromuscular inhibition. On an extraocular muscle of the rabbit (responding to depolarizing agents by contraction) epibatidine in vitro and in situ caused a contraction at a 100-fold lower dose than suxamethonium. The Straub tail reaction in mice to epibatidine could be attributed to the sustained stimulation of motor end plate receptors of the "slow contracting" type of muscle fibres by epibatidine. Epibatidine was the most potent agonist on all neuronal and neuromuscular nicotinic receptors examined.