Pyridostigmine bromide 10mg tablets
Requires a prescription from a doctor or prescriber
Medication used to treat myasthenia gravis
Official documents, adverse reaction reporting, and safety monitoring
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Safety monitoring data
Yellow Card reports
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Suspected adverse reactions reported for Pyridostigmine
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
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Suspected adverse reactions reported for Pyridostigmine
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
Part of the Mestinon brand family (generic: Pyridostigmine)
MHRA licensed products
View all licensed products for Pyridostigmine on the MHRA register
WHO defined daily dose (DDD)
180 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary BNF/ATC mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(3)
Parkinson's disease in adults (NG71)
Efgartigimod for treating antibody-positive generalised myasthenia gravis (TA1069)
Rozanolixizumab for treating antibody-positive generalised myasthenia gravis (TA1155)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 7 · Randomised trials: 12 · 1979–2026
Showing the 50 most relevant studies, sorted by most relevant.
B. Wilkie, Jawed Noori, M. Johnston, et al.
ANZ Journal of Surgery, 2023
N. Pavic, Shane Zhang, A. Maloof, et al.
Open Heart, 2025
- Hypotension, Orthostatic
- Pyridostigmine Bromide
- Blood Pressure
Schiweck N, Langer K, Maier A, et al.
2026
- Postural Orthostatic Tachycardia Syndrome
Postural orthostatic tachycardia syndrome (POTS) is a condition defined by symptoms of orthostatic intolerance and a sustained heart rate (HR) increment of ≥ 30 beats per minute (bpm) upon postural change to the upright position in the absence of orthostatic hypotension, defined as a sustained decrease in systolic blood pressure (SBP) of ≥ 20 mmHg or a decrease in diastolic blood pressure (DBP) of ≥ 10 mmHg within 3 min of standing. In children, a sustained HR increment of at least 40 bpm is required for diagnosis of POTS. POTS is a common condition in adults and children suffering from myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). In daily clinical practice, therapeutic recommendations are rare and evidence is missing. The objective of this review is to present the current knowledge on non-pharmacological and pharmacological approaches in POTS with a special focus on POTS therapy in children and people with ME/CFS. Of 3853 studies, 45 studies were included in the systematic review. Evidence on therapy in POTS is rare and large randomized controlled trials (RCT) on single interventions are needed. Non-pharmacological approaches such as the use of compression garments, physical training, salt supplementation and transdermal vagal nerve stimulation could be possible treatment options in POTS because they are easy to implement as first-line therapeutic measures in clinical practice. For pharmaceuticals, several studies showed significant effects following therapy with ivabradine and β-adrenergic blocking agents. There are single studies which imply that midodrine (hydrochloride) and pyridostigmine seem to have a beneficial effect on hemodynamics in POTS.
Abstract licence: CC BY
Cocchi C, Rossetti V, Zupin L, et al.
2026
- Intestinal Pseudo-Obstruction
- Neostigmine
- Pyridostigmine Bromide
Sebastian R. Schreglmann, Fabian Büchele, Michael Sommerauer, et al.
European Journal of Neurology, 2017
- Blood Pressure
- Cholinesterase Inhibitors
- Fludrocortisone
L. Traeger, S. Bedrikovetski, T. Fitzsimmons, et al.
The British journal of surgery, 2024
J. Moon, Do-Yong Kim, Woo-Jin Lee, et al.
Neurotherapeutics, 2018
- Adrenergic beta-Antagonists
- Propranolol
- Pyridostigmine Bromide
Remijn-Nelissen L, Bakker WR, van den Hout WB, et al.
2026
- Myasthenia Gravis
- Pyridostigmine Bromide
- Cholinesterase Inhibitors
Jihyun An, Heeyun Noh, Eunju Kim, et al.
Korean journal of anesthesiology, 2019
- Sugammadex
- Cholinesterase Inhibitors
- Neuromuscular Nondepolarizing Agents
K. Jones, C. Burckhardt, A. Deodhar, et al.
Arthritis and rheumatism, 2008
- Anxiety
- Cholinesterase Inhibitors
- Combined Modality Therapy
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
1.86 hours
Mechanism
Myasthenia gravis is an autoimmune disease involving dysfunction at the neuromus…
Food interactions
1 warning
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
10-20%
Half-life
1.86 hours
Protein binding
[A231019][L32418]
Volume of distribution
1.76 L/kg
Metabolism
Elimination
90%
[L32413]
Roughly 90% of an intravenous dose is recovered in the urine within 24 hours, with…
Clearance
1.0 L/h
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Pyridostigmine was granted initial FDA approval on April 6, 1955, as an oral tablet. Possible dose forms have been expanded to include extended-release tablets, syrups, and injections, marketed under various brand and generic names.[L32408][L32413]
[L32408]
When administered intravenously, it is indicated for the reversal or antagonism of the neuromuscular blocking effects of nondepolarizing muscle relaxants.
[L32413]
Pyridostigmine has also been used as a prophylactic agent against irreversible organophosphorus acetylcholinesterase inhibitors, primarily in a military capacity.
[L32418]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 294 interactions
[L32408][L32413]
Pyridostigmine is a reversible acetylcholinesterase inhibitor that increases extracellular acetylcholine levels in the neuromuscular junction by impairing its breakdown by acetylcholinesterase.[L32408][L32413] The increased acetylcholine leads to increased neural transmission across the junction, which drastically improves myasthenia gravis symptoms.[A231004]
In addition to its use in myasthenia gravis and in reversing neuromuscular blocks, pyridostigmine is also a common first-line treatment in congenital myasthenic syndromes (CMS), of which there are multiple subtypes caused by mutations in more than 30 distinct genes.[A231009][A231014] CMS present similarly to myasthenia gravis, albeit due to distinct underlying causes, and often benefit from pyridostigmine. However, in some subgroups, treatment with pyridostigmine is detrimental; detailed genetic testing is required before starting therapy.[A231009][A231014]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A231019][L32418]
Approximately 1-2 hours following a single oral dose of 60 mg, the Cmax was determined to be 40-60 μg/L.
[A231019]
Pyridostigmine follows approximately linear kinetics, with a direct correlation between the dose and plasma AUC.
[A231019]
Pyridostigmine taken orally with food results in a flatter peak to the plasma concentration vs. time curve. The peak plasma concentrations are reached ~90 minutes later than in fasted subjects but with no change in bioavailability or AUC.
[A231024]
[A231019]
[A231019][L32418]
[A231019]
[A231019][L32418]
One study suggested the existence of as many as eight metabolites in the urine of patients receiving radiolabeled pyridostigmine intravenously, including various glucuronidated, demethylated, and oxidized (quinone) metabolites.
[A231029][L32418]
Another study confirmed that HNM is the main metabolite, and suggested additional possible metabolites such as a 3,4- or 3,6-dihydroxy-N-methyl-pyridinium or a methoxy- or acetoxy-N-methyl-pyridinium.
[A231034]
The exact products formed, apart from HNM, require further validation.
[L32413]
Roughly 90% of an intravenous dose is recovered in the urine within 24 hours, with unchanged pyridostigmine and its main metabolite HNM recovered in an approximately 4:1 ratio.
[A231019][A231034][L32418]
[A231019]
Proteins and enzymes this drug interacts with in the body
PMID:22409427
Factor Xa activates pro-inflammatory signaling pathways in a protease-activated receptor (PAR)-dependent manner .
PMID:24041930 PMID:30568593 PMID:34831181 PMID:18202198
Up-regulates expression of protease-activated receptors (PARs) F2R, F2RL1 and F2RL2 in dermal microvascular endothelial cells .
PMID:35738824
Triggers the production of pro-inflammatory cytokines, such as MCP-1/CCL2 and IL6, in cardiac fibroblasts and umbilical vein endothelial cells in PAR-1/F2R-dependent manner .
PMID:30568593 PMID:34831181
Triggers the production of pro-inflammatory cytokines, such as MCP-1/CCL2, IL6, TNF-alpha/TNF, IL-1beta/IL1B, IL8/CXCL8 and IL18, in endothelial cells and atrial tissues .
PMID:24041930 PMID:35738824 PMID:9780208
Induces expression of adhesion molecules, such as ICAM1, VCAM1 and SELE, in endothelial cells and atrial tissues .
PMID:24041930 PMID:35738824 PMID:9780208
Increases expression of phosphorylated ERK1/2 in dermal microvascular endothelial cells and atrial tissues .
PMID:24041930 PMID:35738824
Triggers activation of the transcription factor NF-kappa-B in dermal microvascular endothelial cells and atrial tissues .
PMID:24041930 PMID:35738824
Activates pro-inflammatory and pro-fibrotic responses in dermal fibroblasts and enhances wound healing probably via PAR-2/F2RL1-dependent mechanism .
PMID:18202198
Activates barrier protective signaling responses in endothelial cells in PAR-2/F2RL1-dependent manner; the activity depends on the cleavage of PAR-2/F2RL1 by factor Xa .
PMID:22409427
Up-regulates expression of plasminogen activator inhibitor 1 (SERPINE1) in atrial tissues PMID:24041930
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC N07AA02
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Pyridostigmine
Additional database identifiers
Drugs Product Database (DPD)
6296
ChemSpider
4817
BindingDB
50313079
ZINC
ZINC000000002009
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3528
GenAtlas
F10
GeneCards
F10
GenBank Gene Database
K03194
GenBank Protein Database
182841
Guide to Pharmacology
2359
UniProt Accession
FA10_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:983
GenAtlas
BCHE
GeneCards
BCHE
GenBank Gene Database
M32391
GenBank Protein Database
1311630
Guide to Pharmacology
2471
UniProt Accession
CHLE_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:108
GenAtlas
ACHE
GeneCards
ACHE
GenBank Gene Database
M55040
GenBank Protein Database
177975
Guide to Pharmacology
2465
UniProt Accession
ACES_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:108
GenAtlas
ACHE
GeneCards
ACHE
GenBank Gene Database
M55040
GenBank Protein Database
177975
Guide to Pharmacology
2465
UniProt Accession
ACES_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:983
GenAtlas
BCHE
GeneCards
BCHE
GenBank Gene Database
M32391
GenBank Protein Database
1311630
Guide to Pharmacology
2471
UniProt Accession
CHLE_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
DrugBank citations
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q419472), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.