Pyridostigmine BromideCAS# 101-26-8 |
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| Cas No. | 101-26-8 | SDF | Download SDF |
| PubChem ID | 7550 | Appearance | Powder |
| Formula | C9H13BrN2O2 | M.Wt | 261.12 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | H2O : 8.8 mg/mL (33.70 mM; Need ultrasonic and warming) | ||
| Chemical Name | (1-methylpyridin-1-ium-3-yl) N,N-dimethylcarbamate;bromide | ||
| SMILES | [Br-].CN(C)C(=O)Oc1ccc[n+](C)c1 | ||
| Standard InChIKey | VNYBTNPBYXSMOO-UHFFFAOYSA-M | ||
| Standard InChI | InChI=1S/C9H13N2O2.BrH/c1-10(2)9(12)13-8-5-4-6-11(3)7-8;/h4-7H,1-3H3;1H/q+1;/p-1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Pyridostigmine is a parasympathomimetic and a reversible cholinesterase inhibitor.
Target: AChE
Pyridostigmine is a parasympathomimetic and a reversible cholinesterase inhibitor. Since it is a quaternary amine, it is poorly absorbed in the gut and does not cross the blood–brain barrier, except possibly in stressful conditions. Pyridostigmine inhibits acetylcholinesterase in the synaptic cleft, thus slowing down the hydrolysis of acetylcholine. It is a quaternary carbamate inhibitor of cholinesterase that does not cross the blood–brain barrier which carbamylates about 30% of peripheral cholinesterase enzyme. The carbamylated enzyme eventually regenerates by natural hydrolysis and excess ACh levels revert to normal.
Pyridostigmine is used to treat muscle weakness in people with myasthenia gravis and to combat the effects of curariform drug toxicity. Pyridostigmine bromide has been FDA approved for military use during combat situations as an agent to be given prior to exposure to the nerve agent Soman in order to increase survival. Used in particular during the first Gulf War, pyridostigmine bromide has been implicated as a causal factor in Gulf War syndrome. Pyridostigmine sometimes is used to treat orthostatic hypotension. It may also be of benefit in chronic axonal polyneuropathy. References: | |||||
Pyridostigmine Bromide Dilution Calculator
Pyridostigmine Bromide Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.8297 mL | 19.1483 mL | 38.2966 mL | 76.5931 mL | 95.7414 mL |
| 5 mM | 0.7659 mL | 3.8297 mL | 7.6593 mL | 15.3186 mL | 19.1483 mL |
| 10 mM | 0.383 mL | 1.9148 mL | 3.8297 mL | 7.6593 mL | 9.5741 mL |
| 50 mM | 0.0766 mL | 0.383 mL | 0.7659 mL | 1.5319 mL | 1.9148 mL |
| 100 mM | 0.0383 mL | 0.1915 mL | 0.383 mL | 0.7659 mL | 0.9574 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Pyridostigmine is a parasympathomimetic and a reversible cholinesterase inhibitor.
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Persistent modification of Nav1.9 following chronic exposure to insecticides and pyridostigmine bromide.[Pubmed:24732443]
Toxicol Appl Pharmacol. 2014 Jun 15;277(3):298-309.
Many veterans of the 1991 Gulf War (GW) returned from that conflict with a widespread chronic pain affecting deep tissues. Recently, we have shown that a 60day exposure to the insecticides permethrin, chlorpyrifos, and Pyridostigmine Bromide (NTPB) had little influence on nociceptor action potential forming Nav1.8, but increased Kv7 mediated inhibitory currents 8weeks after treatment. Using the same exposure regimen, we used whole cell patch methods to examine whether the influences of NTPB could be observed on Nav1.9 expressed in muscle and vascular nociceptors. During a 60day exposure to NTPB, rats exhibited lowered muscle pain thresholds and increased rest periods, but these measures subsequently returned to normal levels. Eight and 12weeks after treatments ceased, DRG neurons were excised from the sensory ganglia. Whole cell patch studies revealed little change in voltage dependent activation and deactivation of Nav1.9, but significant increases in the amplitude of Nav1.9 were observed 8weeks after exposure. Cellular studies, at the 8week delay, revealed that NTPB also significantly prolonged action potential duration and afterhyperpolarization (22 degrees C). Acute application of permethrin (10muM) also increased the amplitude of Nav1.9 in skin, muscle and vascular nociceptors. In conclusion, chronic exposure to Gulf War agents produced long term changes in the amplitude of Nav1.9 expressed in muscle and vascular nociceptors. The reported increases in Kv7 amplitude may have been an adaptive response to increased Nav1.9, and effectively suppressed behavioral pain measures in the post treatment period. Factors that alter the balance between Nav1.9 and Kv7 could release spontaneous discharge and produce chronic deep tissue pain.
Pyridostigmine bromide versus fludrocortisone in the treatment of orthostatic hypotension in Parkinson's disease - a randomized controlled trial.[Pubmed:28224720]
Eur J Neurol. 2017 Apr;24(4):545-551.
BACKGROUND AND PURPOSE: Evidence for effective treatment options for orthostatic hypotension (OH) in Parkinson's disease (PD) is scarce. Elevation of cholinergic tone with Pyridostigmine Bromide has been reported as a way to improve blood pressure (bp) regulation in neurogenic hypotension without causing supine hypertension. METHODS: This was a double-centre, double-blind, randomized, active-control, crossover, phase II non-inferiority trial of Pyridostigmine Bromide for OH in PD (clinicaltrials.gov NCT01993680). Patients with confirmed OH were randomized to 14 days 3 x 60 mg/day Pyridostigmine Bromide or 1 x 0.2 mg/day fludrocortisone before crossover. Outcome was measured by peripheral and central bp monitoring during the Schellong manoeuvre and questionnaires. RESULTS: Thirteen participants were enrolled between April 2013 and April 2015 with nine participants completing each trial arm. Repeated measures comparison showed a significant 37% improvement with fludrocortisone for the primary outcome diastolic bp drop on orthostatic challenge (baseline 22.9 +/- 13.6 vs. Pyridostigmine Bromide 22.1 +/- 17.0 vs. fludrocortisone 14.0 +/- 12.6 mmHg; P = 0.04), whilst Pyridostigmine Bromide had no effect. Fludrocortisone caused an 11% peripheral systolic supine bp rise (baseline 128.4 +/- 12.8 vs. Pyridostigmine Bromide 130.4 +/- 18.3 vs. fludrocortisone 143.2 +/- 10.1 mmHg; P = 0.01) but no central mean arterial supine bp rise (baseline 107.2 +/- 7.8 vs. Pyridostigmine Bromide 97.0 +/- 12.0 vs. fludrocortisone 107.3 +/- 6.3 mmHg; P = 0.047). Subjective OH severity, motor score and quality of life remained unchanged by both study interventions. CONCLUSIONS: Pyridostigmine Bromide is inferior to fludrocortisone in the treatment of OH in PD. This trial provides first objective evidence of the efficacy of 0.2 mg/day fludrocortisone for OH in PD, causing minor peripheral but no central supine hypertension. In addition to peripheral bp, future trials should include central bp measurements, known to correlate more closely with cardiovascular risk.
Effects of cholinergic stimulation with pyridostigmine bromide on chronic chagasic cardiomyopathic mice.[Pubmed:25221388]
Mediators Inflamm. 2014;2014:475946.
The aim of the present study was to assess the effects of an anticholinesterase agent, Pyridostigmine Bromide (Pyrido), on experimental chronic Chagas heart disease in mice. To this end, male C57BL/6J mice noninfected (control:Con) or chronically infected (5 months) with Trypanosoma cruzi (chagasic:Chg) were treated or not (NT) with Pyrido for one month. At the end of this period, electrocardiogram (ECG); cardiac autonomic function; heart histopathology; serum cytokines; and the presence of blood and tissue parasites by means of immunohistochemistry and PCR were assessed. In NT-Chg mice, significant changes in the electrocardiographic, autonomic, and cardiac histopathological profiles were observed confirming a chronic inflammatory response. Treatment with Pyrido in Chagasic mice caused a significant reduction of myocardial inflammatory infiltration, fibrosis, and hypertrophy, which was accompanied by a decrease in serum levels of IFNgamma with no change in IL-10 levels, suggesting a shift of immune response toward an anti-inflammatory profile. Lower nondifferent numbers of parasite DNA copies were observed in both treated and nontreated chagasic mice. In conclusion, our findings confirm the marked neuroimmunomodulatory role played by the parasympathetic autonomic nervous system in the evolution of the inflammatory-immune response to T. cruzi during experimental chronic Chagas heart disease in mice.
