188125-42-0

188125-42-0 structure

Name: Zolunicant
Chemical Name: Zolunicant
CAS Number: 188125-42-0
Molecular Formula: C₂₂H₂₈N₂O₃
Molecular Weight: 368.47
Catalog: Signaling Pathways Membrane Transporter/Ion Channel nAChR
Create Date: 2022-10-06 11:08:44
Modify Date: 2024-04-08 12:35:17
Zolunicant (MM-110) is a potent inhibitor against nicotinic α3β4 receptors with an IC50 of 0.90 μM to combat addiction. Zolunicant can decrease the self-administration of several addictive agents including morphine, cocaine, methamphetamine, nicotine, and ethanol in rat model. Zolunicant can be studied as a potential treatment for multiple forms of drug abuse[1]. Zolunicant also reveals a potent leishmanicide effect against Leishmania amazonensis[2].

Name	Zolunicant

Description	Zolunicant (MM-110) is a potent inhibitor against nicotinic α3β4 receptors with an IC50 of 0.90 μM to combat addiction. Zolunicant can decrease the self-administration of several addictive agents including morphine, cocaine, methamphetamine, nicotine, and ethanol in rat model. Zolunicant can be studied as a potential treatment for multiple forms of drug abuse[1]. Zolunicant also reveals a potent leishmanicide effect against Leishmania amazonensis[2].
Related Catalog	Research Areas >> Infection Signaling Pathways >> Membrane Transporter/Ion Channel >> nAChR Signaling Pathways >> Neuronal Signaling >> nAChR Research Areas >> Neurological Disease
Target	IC50: 0.90 μM (nicotinic α3β4 receptor)[1]
In Vitro	Zolunicant (18-MC; 0.01-100 μM) shows an inhibitory activity against nicotinic α3β4 receptors with an IC50 of 0.90 μM[1]. . Zolunicant (18-MCOR; 0-20 μg/ml; 24h) also shows antiamastigote activity against L. amazonensis-infected macrophage[2]. Cell Viability Assay[2] Cell Line: L. amazonensis-infected macrophage Concentration: 0, 1, 10,15 and 20 μg/ml Incubation Time: 24 h Result: Decreased the amastigote survival by 73, 84, and 92%, respectively in the treatment with 18-MCOR at 1, 10, or 20 μg/ml.
In Vivo	Zolunicant (18-MC; Intravenous administration; 0-20 μg a day;14 days) decreases morphine self-administration by blocking α3β4 nicotinic receptors in the habenulo-interpeduncular pathway[3]. Animal Model: Naïve female Long-Evans derived rats[3] Dosage: 0,10 and 20 μg Administration: Intravenous administration; once a day; 14 days Result: Infused into the medial habenula and interpeduncular nucleus decreased morphine self-administration (interpeduncular nucleus: F(5,29) = 6.89, P < 0.0001; medial habenula: F(4,28) = 3.07, P < 0.03).
References	[1]. Pace CJ, et al. Novel iboga alkaloid congeners block nicotinic receptors and reduce drug self-administration. European journal of pharmacology. 2004;492(2-3):159-67. [2]. Delorenzi JC, et al. In vitro activities of iboga alkaloid congeners coronaridine and 18-methoxycoronaridine against Leishmania amazonensis. Antimicrob Agents Chemother. 2002;46(7):2111-5. [3]. Glick SD, et al. 18-Methoxycoronaridine acts in the medial habenula and/or interpeduncular nucleus to decrease morphine self-administration in rats. European journal of pharmacology. 2006;537(1-3):94-8.

Molecular Formula	C₂₂H₂₈N₂O₃
Molecular Weight	368.47

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