GZ-793A

GZ-793A is an orally active and selective vesicular monoamine transporter-2 (VMAT2) inhibitor, with an Ki of 0.029 µM. GZ-793A inhibits the neurochemical effects of methamphetamine (METH)-induced dopamine release. GZ-793A can be used for research of METH addiction[1][2][3].

Research Areas >> Neurological Disease

Signaling Pathways >> Membrane Transporter/Ion Channel >> Monoamine Transporter

Ki: 0.029 µM (VMAT2)[1].

GZ-793A (30, 60, 120 or 240 mg/kg; p.o.; once) decreases the number of METH infusions self-administered across each time interval evaluats in a dose-dependent manner[1]. GZ-793A (1-100 µM; 90 min) inhibits METH (5 µM)-evoked fractional dopamine releases[2]. Animal Model: Adult male Sprague-Dawley rats[1]. Dosage: 30, 60, 120 or 240 mg/kg Administration: Oral administration; once. Result: Decreased the number of METH infusions self-administered in a dose-dependent manner, and with an ~85% reduction at the highest dose (240 mg/kg). Decreased the METH self-administration produced by lasted at least 180 min. Animal Model: Male Sprague-Dawley rats (250–275 g; 9-week-old; 0.5 mm thick rats coronal striatal slices are used)[2]. Dosage: 1-100 µM Administration: 90 min Result: Inhibited methamphetamine-evoked dopamine released in a concentration-dependent manner.

[1]. Wilmouth CE, et al. Oral administration of GZ-793A, a VMAT2 inhibitor, decreases methamphetamine self-administration in rats. Pharmacol Biochem Behav. 2013 Nov;112:29-33.

[2]. Nickell JR, et al. GZ-793A inhibits the neurochemical effects of methamphetamine via a selective interaction with the vesicular monoamine transporter-2. Eur J Pharmacol. 2017 Jan 15;795:143-149.

[3]. Nickell JR, et al. The vesicular monoamine transporter-2: an important pharmacological target for the discovery of novel therapeutics to treat methamphetamine abuse. Adv Pharmacol. 2014;69:71-106.