Ziconotide acetate (SNX-111 acetate), a peptide, is a potent and selective block of N-type calcium channels antagonist. Ziconotide acetate reduces synaptic transmission, and can be used for chronic pain research[1].
Most native cells express a variety of different calcium channels and as a result, Ziconotide acetate only partially reduces high-voltage-activated calcium currents in differentiated human neuroblastoma IMR32 cells, rat superior cervical ganglion neurons, and rat hippocampal neurons. Ziconotide acetate also reduces calcium currents that result from expression of the α1B subunit in HEK cells, tsa-201 cells, and Xenopus laevis oocytes[1].Ziconotide acetate delivers its antinociceptive efficacy by reducing the release of pronociceptive neurotransmitters in the dorsal horn of the spinal cord, thereby inhibiting pain signal transmission[1].
Ziconotide (i.t.; 25-100 pmol/site; 5 μL; on the 4 th, 10 th, 15 th, 20 th, and 24 th days) acetate reduces the levels of IL-1β and IL-23 in the CNS, as well as IL-17 production in the spleen, 25 days after MOG35-55-elicited EAE, in the mouse model of experimental autoimmune encephalomyelitis (EAE)[2].
[1]. Joseph G McGivern, et al. Ziconotide: a review of its pharmacology and use in the treatment of pain. Neuropsychiatr Dis Treat. 2007 Feb;3(1):69-85.
[2]. Rodrigo B M Silva, et al. Beneficial Effects of the Calcium Channel Blocker CTK 01512-2 in a Mouse Model of Multiple Sclerosis. Mol Neurobiol. 2018 Dec;55(12):9307-9327.