Potassium bromide 850mg tablets
Requires a prescription from a doctor or prescriber
A white crystal or crystalline powder used as an electrolyte replenisher, in the treatment of hypokalemia, in buffer solutions, and in fertilizers and explosives.
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Official medicine documents
Safety monitoring data
Yellow Card reports
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Suspected adverse reactions reported for Potassium bromide
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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 Potassium bromide
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1 branded products available
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(1)
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
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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.
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 all 28 studies.
Reviews & meta-analyses: 1 · 1928–2026
Showing all 28 studies, sorted by most relevant.
Hope E Baird-Heinz, A'ndrea L Van Schoick, F. Pelsor, et al.
Journal of the American Veterinary Medical Association, 2012
- Anticonvulsants
- Bromides
- Dog Diseases
Jun‐Nan Yang, Yang Song, Jisong Yao, et al.
Journal of the American Chemical Society, 2020
By W. L. T. Addison
Canadian Medical Association journal, 1928
- Hypertension
- Potassium
- History, 20th Century
Kashinath R. Patil, Atri D. Tripathi, Gopal Pathak, et al.
Journal of Chemical & Engineering Data, 1991
Hao Lin, Qi Wei, K. Ng, et al.
Small, 2021
Qi Li, M. M. Haque, V. Kuzmenko, et al.
Journal of Power Sources, 2017
Sadeer M. Majeed, D. Ahmed, Mustafa K. A. Mohammed
Organic Electronics, 2021
Zunhong Chen, Junhong Jin, Shenglin Yang, et al.
Journal of Materials Chemistry A, 2024
Li S, Xie X, Liu Y
2024
Non-photochemical laser-induced nucleation (NPLIN) in supersaturated potassium bromide (KBr) solutions with the addition of acidic polymers is reported here for the first time. Upon absorbing the incident laser, crystallites are immediately induced along the laser pathway in the solution, eventually growing into needle-shaped crystals of varying sizes. When comparing induction time, nucleation probability, and crystal habits with spontaneous nucleation, the results suggest that NPLIN creates a distinct morphological pathway, transforming cubic crystals into needle-like structures. Additionally, it improves crystallization probability and growth rate. This paper aims to realize control from crystal nucleation to crystal growth by adding acidic polymers to the process of laser-induced nucleation, potentially influencing crystal morphology modification in NPLIN. With 19 wt% acidic polymers added to the solution as additives, control over both crystal growth and morphological modifications was observed: cubic KBr crystals with square patterns were produced through laser irradiation, and there was a varying reduction in both the number and growth rate of the crystals. The influence of acidic polymers on the solution environment was analyzed to determine the reasons for the variations in crystal quantity and growth speed. The underlying mechanisms responsible for the changes in crystal shape were also discussed.
Abstract licence: CC BY
Pringsheim M, Kluger G, Strzelczyk A, et al.
2025
- Anticonvulsants
- Bromides
- Epilepsies, Myoclonic
OBJECTIVE: To assess the efficacy and tolerability of fenfluramine (FFA) with concomitant potassium bromide (BR) in patients with Dravet syndrome (DS). METHODS: This multicenter retrospective study, conducted within the German compassionate use program, analyzed BR doses and serum levels before and after FFA initiation, adverse events (AEs), seizure reduction, and symptoms changes using the Clinical Global Impression of Change (CGIC) scale. Timepoints were defined as T0 (baseline), T1 (FFA initiation), T2 and T3 (first and second BR level measurement after FFA initiation). RESULTS: Twenty-two patients (median age 8.9 years, range 2.2-26.7) treated with BR were included. Median duration of BR-FFA combination therapy was 7 months (range 0-28). BR doses were reduced at least once in 11 patients (50%) as a precaution or because of increased serum levels. At T3, mean BR dose was significantly lower compared to T0 (1217 mg/day, SD = 699 vs. 1755 mg/day, SD = 752.2; p = 0.04), but BR levels showed no significant difference between T2 or T3 and baseline. In contrast, for patients with stable BR doses (n = 14), mean BR level significantly increased from baseline (1376 mg/L, SD = 345.7) to T2 (1762 mg/L, SD = 553.3; p = 0.04). AEs were reported in 15 patients (68.2%) during the combination therapy, with the most common being somnolence (59.1%) and loss of appetite (22.7%). In 40.9% either FFA or BR were discontinued due to sedation. The responder rate for seizure reduction was 68.4% at 3 months and 76.9% at 6 months. SIGNIFICANCE: BR levels increased significantly after FFA initiation when BR doses were not reduced, contributing to adverse events-primarily somnolence-and resulting in the discontinuation of BR or FFA in some patients. Close monitoring of BR levels is crucial to minimize the risk of adverse events. PLAIN LANGUAGE SUMMARY: This study investigated the combination of fenfluramine (FFA) and potassium BR in treating Dravet syndrome. It was found that it is effective in reducing seizures, but BR levels often went up after starting FFA, which caused side effects like drowsiness in many patients. In some cases, these side effects were serious enough that physicians had to stop either BR or FFA. The study highlights the need for careful monitoring of BR levels when using this combination to avoid potential side effects by reducing the BR dose early if needed.
Abstract licence: CC BY-NC-ND
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
Not available
Mechanism
Supplemental potassium in the form of high potassium food or potassium chloride…
Food interactions
2 warnings
Human targets
6 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Elimination
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
The FDA withdrew its approval for the use of all solid oral dosage form drug products containing potassium chloride that supply 100 mg or more of potassium per dosage unit, except for controlled-release dosage forms and those products formulated for preparation of solution prior to ingestion.[L43942]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 955 interactions
Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9-12 mEq/L).
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:16669787 PMID:32081947 PMID:32294086 PMID:33597714 PMID:35585053 PMID:36239040 PMID:36306358 PMID:7629105
Plays a vital role in the regulation of ionic balance and cell volume PMID:16669787 PMID:32081947 PMID:32294086 PMID:7629105
PMID:21321328
Electrically silent transporter system (By similarity)
PMID:12106695
As major extruder of intracellular chloride, it establishes the low neuronal Cl(-) levels required for chloride influx after binding of GABA-A and glycine to their receptors, with subsequent hyperpolarization and neuronal inhibition (By similarity). Involved in the regulation of dendritic spine formation and maturation PMID:24668262
PMID:10600773 PMID:11551954 PMID:16048901 PMID:18566107 PMID:19665974 PMID:21628467 PMID:27485015
May contribute to cell volume homeostasis in single cells PMID:16048901 PMID:27485015
PMID:10913127
May mediate K(+) uptake into Deiters' cells in the cochlea and contribute to K(+) recycling in the inner ear. Important for the survival of cochlear outer and inner hair cells and the maintenance of the organ of Corti. May be required for basolateral Cl(-) extrusion in the kidney and contribute to renal acidification (By similarity)
Proteins that transport this drug across cell membranes
PMID:16669787 PMID:32081947 PMID:32294086 PMID:33597714 PMID:35585053 PMID:36239040 PMID:36306358 PMID:7629105
Plays a vital role in the regulation of ionic balance and cell volume PMID:16669787 PMID:32081947 PMID:32294086 PMID:7629105
PMID:21321328
Electrically silent transporter system (By similarity)
PMID:12106695
As major extruder of intracellular chloride, it establishes the low neuronal Cl(-) levels required for chloride influx after binding of GABA-A and glycine to their receptors, with subsequent hyperpolarization and neuronal inhibition (By similarity). Involved in the regulation of dendritic spine formation and maturation PMID:24668262
PMID:10600773 PMID:11551954 PMID:16048901 PMID:18566107 PMID:19665974 PMID:21628467 PMID:27485015
May contribute to cell volume homeostasis in single cells PMID:16048901 PMID:27485015
PMID:10913127
May mediate K(+) uptake into Deiters' cells in the cochlea and contribute to K(+) recycling in the inner ear. Important for the survival of cochlear outer and inner hair cells and the maintenance of the organ of Corti. May be required for basolateral Cl(-) extrusion in the kidney and contribute to renal acidification (By similarity)
PMID:35759661
May contribute to cell volume homeostasis in single cells .
PMID:10913127 PMID:34031912
May be involved in the regulation of basolateral Cl(-) exit in NaCl absorbing epithelia (By similarity)
ATC B05XA01
ATC A12BA01
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)
Potassium chloride
Matched from: Potassium bromide
Additional database identifiers
Drugs Product Database (DPD)
53
Drugs Product Database (DPD)
11393
Drugs Product Database (DPD)
4608
Drugs Product Database (DPD)
4959
Drugs Product Database (DPD)
6485
ChemSpider
4707
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10911
GenAtlas
SLC12A2
GeneCards
SLC12A2
GenBank Gene Database
U30246
GenBank Protein Database
903682
Guide to Pharmacology
969
UniProt Accession
S12A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10910
GenAtlas
SLC12A1
GeneCards
SLC12A1
GenBank Gene Database
U58130
GenBank Protein Database
1373425
Guide to Pharmacology
968
UniProt Accession
S12A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:13818
GenAtlas
SLC12A5
GeneCards
SLC12A5
GenBank Gene Database
AF208159
GenBank Protein Database
12003227
Guide to Pharmacology
972
UniProt Accession
S12A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10914
GenAtlas
SLC12A6
GeneCards
SLC12A6
GenBank Gene Database
AF116242
GenBank Protein Database
6693798
UniProt Accession
S12A6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10915
GenAtlas
SLC12A7
GeneCards
SLC12A7
GenBank Gene Database
AF105365
GenBank Protein Database
5106521
UniProt Accession
S12A7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10913
GenAtlas
SLC12A4
GeneCards
SLC12A4
GenBank Gene Database
U55054
GenBank Protein Database
1399212
UniProt Accession
S12A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10911
GenAtlas
SLC12A2
GeneCards
SLC12A2
GenBank Gene Database
U30246
GenBank Protein Database
903682
Guide to Pharmacology
969
UniProt Accession
S12A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10910
GenAtlas
SLC12A1
GeneCards
SLC12A1
GenBank Gene Database
U58130
GenBank Protein Database
1373425
Guide to Pharmacology
968
UniProt Accession
S12A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:13818
GenAtlas
SLC12A5
GeneCards
SLC12A5
GenBank Gene Database
AF208159
GenBank Protein Database
12003227
Guide to Pharmacology
972
UniProt Accession
S12A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10914
GenAtlas
SLC12A6
GeneCards
SLC12A6
GenBank Gene Database
AF116242
GenBank Protein Database
6693798
UniProt Accession
S12A6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10915
GenAtlas
SLC12A7
GeneCards
SLC12A7
GenBank Gene Database
AF105365
GenBank Protein Database
5106521
UniProt Accession
S12A7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10913
GenAtlas
SLC12A4
GeneCards
SLC12A4
GenBank Gene Database
U55054
GenBank Protein Database
1399212
UniProt Accession
S12A4_HUMAN
DrugBank citations
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Structured knowledge from the free knowledge base
Molecular structure

Linked open data from Wikidata (Q184630), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. Molecular structure images from Wikimedia Commons.