Mambalgin-1 vs RgIA
Head-to-head comparison of Mambalgin-1 (Mambalgin-1 from Dendroaspis polylepis venom) and RgIA (alpha-Conotoxin RgIA from Conus regius venom) — benefits, dosing, side effects, research data, and where to buy.
Research Score
| Property | Mambalgin-1 | RgIA |
|---|---|---|
| Category | Experimental | Experimental |
| Full Name | Mambalgin-1 from Dendroaspis polylepis venom | alpha-Conotoxin RgIA from Conus regius venom |
| Molecular Weight | 6,300 Da | 1,670 Da |
| Half-Life | Minutes to hours | Minutes to hours |
| Amino Acids | 57 | 13 |
| Typical Dose | 0.1-1 nmol intrathecal|10-100 nM in vitro|single-dose rodent studies | 10-300 pmol intrathecal|1-100 nM in vitro|single-dose rodent studies |
| Route | Intrathecal | Intrathecal |
| Purity | ≥98% | ≥98% |
| Studies Count | 55 | 130 |
| Research Status | Pre-clinical | Pre-clinical |
Mambalgin-1 Benefits
- ✓ASIC channel inhibition
- ✓non-opioid analgesia research
- ✓sensory-neuron physiology
- ✓lead optimization for pain therapeutics
RgIA Benefits
- ✓alpha9alpha10 nAChR selectivity
- ✓neuropathic pain model tool
- ✓neuroimmune signaling research
- ✓analgesic lead discovery
Mambalgin-1 Dosing
Intrathecal pain-behavior studies|ASIC1a/ASIC1b electrophysiology|Acute dosing in rodents
RgIA Dosing
Intrathecal bolus in rodent pain models|Patch-clamp assays on alpha9alpha10 receptors|Single-dose pre-clinical screening
Mambalgin-1 Side Effects
- ⚠Hypoactivity at high dose
- ⚠off-target ASIC blockade
- ⚠local irritation
RgIA Side Effects
- ⚠Transient autonomic effects
- ⚠off-target nicotinic blockade
- ⚠injection-site irritation
Research Overview
Mambalgin-1
Pre-clinical work shows mambalgin-1 can reduce pain behaviors by modulating proton-gated ion channels in peripheral and central pathways. It has become an important template for developing ASIC-targeted analgesics.
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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