ω-conotoxin SO-3 is a selective blocker of N-type voltage-sensitive calcium channels. EC50 for ω-conotoxin SO-3 is 0.16 µM (similar to ω-conotoxin MVIIA) on HVA calcium currents. ω-conotoxin SO-3 did not show any inhibiting effects on L-type, P/Q-type and R-type currents at 3 µM concentration. ω-conotoxin SO-3 has no effect on voltage-sensitive sodium currents, delayed rectifier potassium currents and transient outward potassium currents. At 3 µM, the inhibition amounts of HVA ICa was very similar between ω-conotoxin SO-3 and ω-conotoxin MVIIA (~ 32%). Their inhibitory effects are almost fully reversible but their half-time for recovery are different (~ 7.5 min for ω-conotoxin SO-3 and ~ 4.14 min for ω-conotoxin MVIIA). ω-conotoxin SO-3 displays an analgesic potency similar to ω-conotoxin MVIIA in a range of acute and chronic pain models in rodents, but has less adverse effects compared with identical dosages of ω-conotoxin MVIIAinjected intrathecally.
Product code: 08CON013.
Categories: Calcium channels, High voltage-gated Ca2+ channels.
Tags: Cav2.2, N-type.
AA sequence: Cys1-Lys-Ala-Ala-Gly-Lys-Pro-Cys8-Ser-Arg-Ile-Ala-Tyr-Asn-Cys15-Cys16-Thr-Gly-Ser-Cys20-Arg-Ser-Gly-Lys-Cys25-NH2
Disulfide bonds: Cys1-Cys16, Cys8-Cys20 and Cys15-Cys25
Length (aa): 25
Formula: C100H166N36O31S6
Molecular Weight: 2561.00 Da
Appearance: White lyophilized solid
Solubility: water and saline buffer
CAS number:
Source: Synthetic
Purity rate: > 97 %
Whole-cell currents in cultured hippocampal neurons were recorded to investigate the effects of SO-3, a new O-superfamily conopeptide derived from Conus striatus, on voltage-sensitive channels. SO-3 had no effect on voltage-sensitive sodium currents, delayed rectifier potassium currents, and transient outward potassium currents. Similar to the selective N-type calcium channel blocker omega-conotoxin MVIIA (MVIIA), SO-3 could concentration-dependently inhibit the high voltage-activated (HVA) calcium currents (I(Ca)). MVIIA(3 microM), 10 microM nimodipine, and 0.5 microM omega-agatoxin IVA (Aga) could selectively block the N-, L-, and P/Q-type I(Ca), which contributed approximately 32, approximately 38, and approximately 21% of the HVA currents in hippocampal neurons, respectively. About 31% of the total HVA currents were inhibited by 3 microM SO-3. SO-3 (3 microM) and 3 microM MVIIA inhibited the overlapping components of HVA currents, whereas no overlapping component was inhibited by 3 microM SO-3 and 10 microM nimodipine, or by 3 microM SO-3 and 0.5 microM Aga. Also, 3 microM SO-3 had no effect on R-type currents. SO-3 had less inhibitory effects on non-N-type HVA currents than MVIIA at higher concentrations (30 and 100 microM). The inhibitory effects of SO-3 and MVIIA on HVA currents were almost fully reversible. However, the recovery from block by MVIIA was more rapid than recovery from block by SO-3. It is concluded that SO-3 is a new omega-conotoxin selectively targeting N-type voltage-sensitive calcium channels. Considering the significance of N-type calcium channels for pain transduction, SO-3 may have therapeutic potential as a novel analgesic agent.
Wen, L., et al. (2005) SO-3, a new O-superfamily conopeptide derived from Conus striatus, selectively inhibits N-type calcium currents in cultured hippocampal neurons, Br J Pharmacol. PMID: 15880145
The effects of a new O-superfamily conotoxin SO3 on sodium and potassium currents were examined in cultured rat hippocampal neurons using the whole-cell patch clamp technique. SO3 caused a concentration-dependent, rapidly developing and reversible inhibition of sodium currents (I(Na)). The IC(50) value for the blockage of I(Na) was calculated to be 0.49 and the Hill coefficient was 1.7. Using electrophysiological and pharmacological protocols, transient A-type potassium currents (I(A)) and delayed rectifiers potassium currents (I(K)) were isolated. SO3 caused a concentration-dependent, and reversible inhibition of I(K). The IC(50) value for the blockage of I(K) was calculated to be 1.6 and the Hill coefficient was 0.6, with no significant effect on I(A). These results indicate that SO3 can selectively inhibit neuronal sodium and potassium currents.Li, Z., et al. (2003) Effect of new O-superfamily conotoxin SO3 on sodium and potassium currents of cultured hippocampal neurons, Brain Res. PMID: 12591132
Smartox生物素ProTx-I电压门控钠通道和T型Cav的阻断剂毒素I（ProTx-1；β-theraphotoxin-Tp1a） 是一种毒素，最初是从Prixopelma pruriens（秘鲁绿色天鹅绒狼蛛）的毒液中分离出来的。此毒素可逆地抑制抗河豚毒素（TTX）的通道 Na v 1.8（IC 50 = 27 nM）和 Na v 1.2，Na v 1.5和Na v 1.7 ，IC 50 值为50至100 nM。此外， ProTx-I 改变了T型Ca v 3.1通道的电压依赖性活动 （IC 50 = 50 nM），而不会影响灭活的电压依赖性。生物素ProTx-I是ProTx-I的生物素标签版本。
