SNX-482 vs RgIA
Head-to-head comparison of SNX-482 (SNX-482 peptide from Hysterocrates gigas venom) and RgIA (alpha-Conotoxin RgIA from Conus regius venom) — benefits, dosing, side effects, research data, and where to buy.
| Property | SNX-482 | RgIA |
|---|---|---|
| Category | Experimental | Experimental |
| Full Name | SNX-482 peptide from Hysterocrates gigas venom | alpha-Conotoxin RgIA from Conus regius venom |
| Molecular Weight | 4,300 Da | 1,670 Da |
| Half-Life | Minutes to hours | Minutes to hours |
| Amino Acids | 41 | 13 |
| Typical Dose | 0.01-1 nmol intrathecal|1-100 nM in vitro|single-dose electrophysiology studies | 10-300 pmol intrathecal|1-100 nM in vitro|single-dose rodent studies |
| Route | Intrathecal | Intrathecal |
| Purity | ≥98% | ≥98% |
| Studies Count | 85 | 130 |
| Research Status | Pre-clinical | Pre-clinical |
SNX-482 Benefits
- ✓Cav2.3 blockade
- ✓synaptic transmission studies
- ✓excitability mapping
- ✓pain and epilepsy research
RgIA Benefits
- ✓alpha9alpha10 nAChR selectivity
- ✓neuropathic pain model tool
- ✓neuroimmune signaling research
- ✓analgesic lead discovery
SNX-482 Dosing
Patch-clamp Cav2.3 assays|Intrathecal neurophysiology studies|Acute channel-blockade experiments
RgIA Dosing
Intrathecal bolus in rodent pain models|Patch-clamp assays on alpha9alpha10 receptors|Single-dose pre-clinical screening
SNX-482 Side Effects
- ⚠Ataxia at high exposure
- ⚠off-target calcium-channel block
- ⚠cardiovascular effects in animal models
RgIA Side Effects
- ⚠Transient autonomic effects
- ⚠off-target nicotinic blockade
- ⚠injection-site irritation
Research Overview
SNX-482
SNX-482 has been used to dissect R-type calcium currents in neurons and endocrine cells, and to map the role of Cav2.3 in excitability. Its selectivity profile has made it a standard research reagent in channel pharmacology.
RgIA
Scientific studies show RgIA can strongly inhibit alpha9alpha10 nicotinic signaling with high selectivity compared with many other nAChR ligands. It is widely used to probe peripheral sensory pathways and inflammation-linked pain mechanisms.
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