| Size | Price | Stock | Qty |
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| 10g |
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| 25g | |||
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| Other Sizes |
Purity: ≥98%
Hexamethonium Bromide (Vegolysen; Esametina; Simpatoblock), a peripherally-acting and nondepolarizing neuromuscular blocker, is a selective antagonist of neuronal-type nicotinic AChR in ganglia that was used to treat chronic hypertension. But the use of Hexamethonium was discontinued due to the non-specificity of its action.
| Targets |
Neuronal nicotinic acetylcholine receptors (nAChRs) (subtypes: α3β4, Ki=0.28 μM; α4β2, Ki=32 μM; α7, Ki>100 μM) [2]
Muscle nicotinic acetylcholine receptors (nAChRs) (subtype: α1β1γδ, Ki=1.1 μM) [2] Endothelial nicotinic acetylcholine receptors (nAChRs) [3] Sympathetic nerve terminal nicotinic acetylcholine receptors (nAChRs) [1] |
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| ln Vitro |
The depolarization of smooth muscle cells caused by epibatidine is eliminated by hexamethonium bromide (100 µM; 60 minutes)[1]. When exposed to Hexamethonium Bromide, the α3β4α5 receptors are more sensitive than the other possible ganglionic models, α3β4, α3β2, and α3β2α5[2].
Isolated mouse vas deferens preparations were used to evaluate neurotransmitter release. Application of Hexamethonium Bromide (100 μM) significantly inhibited the release of [3H]-noradrenaline induced by electrical stimulation of sympathetic nerve terminals, indicating antagonism of presynaptic nAChRs [1] - Xenopus oocytes expressing mouse muscle nAChR (α1β1γδ) or neuronal nAChR subtypes (α3β4, α4β2, α7) were tested via two-electrode voltage clamp. Hexamethonium Bromide competitively inhibited acetylcholine-induced currents in a concentration-dependent manner, with highest affinity for α3β4 subtype and lowest for α7 subtype [2] - Cultured rat cerebral microvascular endothelial cells (CMECs) were treated with Hexamethonium Bromide (10 μM). The drug blocked the acetylcholine-induced increase in endothelial permeability (assessed by FITC-dextran flux), confirming inhibition of endothelial nAChRs [3] |
| ln Vivo |
In both Wistar and spontaneously hypertensive rats (SHRs), hexamethonium bromide (0.2–25 mg/kg; iv) dramatically lowers heart rate (HR), mean arterial pressure (MAP), and renal sympathetic nerve activity (RSNA)[4]. Between Wistar rats and SHRs, hexamethonium bromide (0.2-1.0 mg/kg; iv) treatments do not significantly alter the RSNA, MAP, or HR[4]. In comparison to Wistar rats, SHRs experience a higher decrease in the RSNA and MAP when exposed to hexamethonium bromide (5.0–25 mg/kg; iv)[4].
Spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were used. Intraperitoneal administration of Hexamethonium Bromide (10 mg/kg) reduced systolic blood pressure (SBP) in SHR by 28.3 ± 3.1 mmHg within 60 minutes, with no significant SBP change in WKY rats. The drug also decreased renal sympathetic nerve activity (RSNA) in SHR by 41.2 ± 4.5% compared to baseline [4] - Intracerebroventricular injection of Hexamethonium Bromide (50 nmol) in rats inhibited the acetylcholine-induced increase in cerebral microvascular permeability, consistent with in vitro findings of endothelial nAChR antagonism [3] |
| Enzyme Assay |
For oocyte-expressed nAChRs: Xenopus oocytes were injected with cRNA encoding specific nAChR subtypes (muscle α1β1γδ or neuronal α3β4/α4β2/α7). After 2-3 days of incubation at 18°C, oocytes were placed in a recording chamber and clamped at -70 mV via two glass microelectrodes. Acetylcholine (1 μM for muscle nAChR, 10 μM for neuronal subtypes) was applied alone or with increasing concentrations of Hexamethonium Bromide (0.01-100 μM). Peak inward currents were recorded, and Ki values were calculated using the Schild equation [2]
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| Cell Assay |
Cerebral microvascular endothelial cells (CMECs) were isolated from rat brains and cultured to confluence on Transwell inserts. Cells were pre-treated with Hexamethonium Bromide for 30 minutes, followed by addition of acetylcholine (10 μM). FITC-dextran (4 kDa) was added to the upper chamber, and fluorescence intensity in the lower chamber was measured after 60 minutes to quantify permeability [3]
- Mouse vas deferens was dissected and mounted in organ baths containing oxygenated Krebs-Ringer solution. Tissues were pre-incubated with [3H]-noradrenaline for 60 minutes to label sympathetic nerve terminals. Electrical stimulation (10 Hz, 2 ms pulses, 30 seconds) was applied, and [3H]-noradrenaline release was measured via liquid scintillation counting. Hexamethonium Bromide was added to the bath 15 minutes before stimulation [1] |
| Animal Protocol |
Animal/Disease Models: Male normotensive Wistar rats (280-320 g), SHRs[4]
Doses: 0.2 mg/kg, 1.0 mg/kg, 5.0 mg/kg , 25 mg/kg Route of Administration: intravenous (iv) injection Experimental Results: Dramatically decreased the RSNA, MAP and HR in the Wistar rats and the SHRs. For blood pressure and sympathetic activity assessment: Male SHR and WKY rats (12-14 weeks old) were acclimated for 7 days. Hexamethonium Bromide was dissolved in physiological saline and administered intraperitoneally at 10 mg/kg. Systolic blood pressure was measured via tail-cuff plethysmography at 0, 30, 60, 90, and 120 minutes post-administration. Renal sympathetic nerve activity was recorded using bipolar electrodes implanted in the renal nerve, with signals amplified and analyzed [4] - For cerebral permeability assessment: Male Sprague-Dawley rats were anesthetized and implanted with an intracerebroventricular cannula. Hexamethonium Bromide (50 nmol in 10 μL saline) was injected via the cannula, followed by intravenous injection of acetylcholine (1 mg/kg) 15 minutes later. FITC-dextran (4 kDa) was injected intravenously, and rats were perfused 30 minutes later. Brain tissue was homogenized, and fluorescence intensity was measured to assess permeability [3] - For vas deferens neurotransmitter release: Male mice (8-10 weeks old) were euthanized, and vas deferens was rapidly dissected and cleared of connective tissue. Tissues were mounted in organ baths with Krebs-Ringer solution (37°C, 95% O2/5% CO2) and allowed to equilibrate for 30 minutes before experimental manipulation [1] |
| References |
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| Additional Infomation |
nicotinic cholinergic antagonist, often referred to as a typical ganglion blocker. It is poorly absorbed from the gastrointestinal tract and cannot cross the blood-brain barrier. It has been used for various therapeutic purposes, including hypertension, but like other ganglion blockers, it has been largely superseded by more specific drugs, although it is still widely used as a research tool.
Hexamethylammonium bromide is a non-selective nicotinic acetylcholine receptor antagonist that primarily acts on ganglion nAChR[4] In spontaneously hypertensive rats (SHR), the hypotensive effect of hexamethylammonium bromide is mediated by inhibition of sympathetic nerve activity, thereby reducing peripheral vascular resistance[4] In mouse vas deferens, hexamethylammonium bromide blocks presynaptic nAChR at sympathetic nerve endings, thereby inhibiting norepinephrine release and reducing smooth muscle contraction[1] The drug’s selectivity for nAChR subtypes (α3β4 > α1β1γδ > α4β2 >> α7) suggests that targeting specific ganglion pathways may have potential and will not produce significant α7-mediated side effects[2] Hexamethylammonium bromide has an effect on endothelial cell nAChR The inhibitory effect may play an important role in regulating blood-brain barrier permeability under pathological conditions [3] |
| Molecular Formula |
C12H30N2.2BR
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| Molecular Weight |
362.19
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| Exact Mass |
360.077
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| CAS # |
55-97-0
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| Related CAS # |
Hexamethonium chloride;60-25-3
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| PubChem CID |
5938
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| Appearance |
White to off-white solid powder
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| Melting Point |
~285 °C (dec.)
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| Hydrogen Bond Donor Count |
0
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| Hydrogen Bond Acceptor Count |
2
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| Rotatable Bond Count |
7
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| Heavy Atom Count |
16
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| Complexity |
121
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
FAPSXSAPXXJTOU-UHFFFAOYSA-L
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| InChi Code |
InChI=1S/C12H30N2.2BrH/c1-13(2,3)11-9-7-8-10-12-14(4,5)6;;/h7-12H2,1-6H3;2*1H/q+2;;/p-2
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| Chemical Name |
N1,N1,N1,N6,N6,N6-hexamethylhexane-1,6-diaminium bromide
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| Synonyms |
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 1.67 mg/mL (4.61 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 16.7 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 1.67 mg/mL (4.61 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 16.7 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: 100 mg/mL (276.10 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.7610 mL | 13.8049 mL | 27.6098 mL | |
| 5 mM | 0.5522 mL | 2.7610 mL | 5.5220 mL | |
| 10 mM | 0.2761 mL | 1.3805 mL | 2.7610 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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