ω-Conotoxin GVIA TFA

ω-Conotoxin GVIA TFA is an inhibitor of the N-type Ca 2+ channel [1] .

Peptide neurotoxin; selectively and reversibly blocks N-type calcium channels (IC50 = 0.15 nM). Reduces (RS)-3,5-DHPG -induced long term depression in vivo.

α-Conotoxin Vc1.1 TFA, a disulfide-bonded peptide derived from Conus victoriae, selectively antagonizes nAChRs. It effectively inhibits the α3α5β2, α3β2, and α3β4 nAChR subtypes with IC50 values of 7.2 μM, 7.3 μM, and 4.2 μM, respectively, while exerting minimal inhibition on other nAChR subtypes. This compound shows promise for research into neuropathic pain. [1] [2]

α-Conotoxin AuIB TFA, a potent selective antagonist of the α3β4 nicotinic acetylcholine receptor (nAChR), effectively inhibits nAChRs expressed in Xenopus oocytes, demonstrating an inhibitory concentration (IC 50) of 0.75 μM [1].

α-Conotoxin MII TFA (α-CTxMII TFA), a peptide consisting of 16 amino acids derived from the venom of Conus magus, selectively inhibits nicotinic acetylcholine receptors (nAChRs) that are composed of α3β2 subunits, demonstrating an inhibitory concentration half-maximal (IC50) value of 0.5 nM. Additionally, it effectively targets β3-containing neuronal nicotinic receptors. [1] [2] [3]

α-Conotoxin PIA TFA, targeting nicotinic acetylcholine receptor (nAChR) subtypes with α6 and α3 subunits, acts as an antagonist. This compound shows promise for research into Parkinson’s disease and schizophrenia [1].

α-Conotoxin PnIA TFA, a potent and selective antagonist of the mammalian α7 nAChR, holds promise for neurological research, particularly in studying neuropathic pain and Alzheimer's disease [1].

ω-Conotoxin MVIIC TFA, a potent blocker of N- and P/Q-type Ca2+ channels, significantly counteracts the suppression of glutamate release mediated by 11-keto-βboswellic acid [1].