(±)-Epibatidine

(±)-Epibatidine (CMI 545) is a neuronal nicotinic acetylcholine receptor (nAChR) agonist that targets brain nicotinic receptors, thereby inhibiting afferent micturition pathways and sensory pathways, consequently suppressing the micturition reflex and mediating antihyperalgesic effects. (±)-Epibatidine can be used in the study of trigeminal neuralgia^[1][2]. In Vivo:(±)-Epibatidine (0.001-1 µg; i.c.v.; single administration within 1 minute) dihydrochloride at a dose of 0.1 µg increased bladder capacity in awake rats, significantly prolonging the micturition interval to 217% of that in the control group without altering micturition pressure^[1].
(±)-Epibatidine (0.001-1 µg; i.c.v.; single administration within 1 minute) dihydrochloride at a dose of 0.1 µg increased bladder capacity in Urethane (HY-B1207)-anesthetized rats, significantly prolonging the voiding interval to 191.3% of that in the control group, without significantly altering voiding pressure^[1].
(±)-Epibatidine (0.001-1 µg; i.v.; single administration) dihydrochloride shortened the voiding interval to 33.6-45.2% of the control group and increased the maximum voiding pressure to 185.5-190.5% of the control group at a dose of 1 µg in anesthetized and conscious rats, whereas low and moderate doses (0.001-0.1 µg) had no significant effect^[1].
(±)-Epibatidine (1.0-5.0 mg/kg; s.c.; single injection; 5 min before formalin) dihydrochloride produced dose-dependent antihyperalgesic effects in both the acute and tonic phases of the facial pain formalin model, with ED₅₀ values of 1.78 and 1.12 mg/kg, respectively^[2].
(±)-Epibatidine (2.5 mg/kg; s.c.; single injection; 5, 15, 30, or 60 min before formalin) dihydrochloride mediated a time-dependent antihyperalgesic effect in the facial pain formalin model, with the significant effect disappearing at 15 min in the acute phase and at 30 min in the tonic phase^[2].