Carteolol 1% eye drops
A beta-adrenergic antagonist used as an anti-arrhythmia agent, an anti-angina agent, an antihypertensive agent, and an antiglaucoma agent.
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
View Drug Analysis Profile
Suspected adverse reactions reported for Carteolol
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
Submit a Yellow Card report to the MHRA
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
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
View EudraVigilance report
Suspected adverse reactions reported for Carteolol
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
14 branded products available
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(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
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
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 all 14 studies.
Reviews & meta-analyses: 1 · 2023–2026
Showing all 14 studies, sorted by most relevant.
Qian Ma, Weiwei Wang
Journal of Medical Case Reports, 2024
- Exome Sequencing
- Antigens, Neoplasm
- Cataract
BACKGROUND: Oculocutaneous albinism is a rare autosomal recessive disorder caused by congenital melanin deficiency, resulting in hypopigmentation of the eyes, hair, and skin. This study included a Chinese family with an oculocutaneous albinism pedigree, in which the proband presented with oculocutaneous albinismcombined with secondary angle closure, which has been rarely reported in previous literature. This article primarily focused on the clinical and genetic examination results of this patient and provided recommendations for ophthalmologist to treat patients with oculocutaneous albinism in clinical practice. CASE PRESENTATION: The proband in this case study is a 53-year-old Chinese male who showed depigmentation of the skin, hair, iris, and fundus, accompanied by photophobia, decreased vision, high intraocular pressure, nystagmus, macular fovea hypoplasia, and cataracts. Owing to the opacity and expansion of the lens, the volume ratio of lens to eyeball was increased, causing crowded anterior segment, bombed iris, and narrowed chamber angle and, ultimately, leading to secondary angle closure. Whole-exome sequencing suggested that the two patients in the pedigree harbored the compound heterozygous variants c.230G > A (p. Arg77Gln) and c.832G > A (p. Arg278*) in the TYR gene, while the healthy member carried the TYR c.230G > A (p. Arg77Gln) variant, which was consistent with the autosomal recessive inheritance pattern and further confirmed the diagnosis was oculocutaneous albinism. On the basis of the above results, the patient was diagnosed with oculocutaneous albinism, senile mature cataract, and secondary angle closure in the right eye and ocular hypertension in the left eye, as well as bilateral nystagmus. Then, the patient was prescribed carteolol eye drops to control intraocular pressure and underwent phacoemulsification and intraocular lens implantation surgery for the right eye. Postoperatively, the patient's intraocular pressure was effectively controlled, and visual acuity improved. CONCLUSION: We report a patient with oculocutaneous albinism combined with cataract and secondary angle closure, and whole-exome sequencing suggested that he harbored TYR gene variants. Comprehensive examinations were important for identifying the causes of angle closure and making proper treatment strategies. Genetic testing enabled precise diagnosis and genetic counseling.
Abstract licence: CC BY-NC-ND
Guo-Jian Jiang, Xinguo You, T. Fan
Chemico-biological interactions, 2023
- Carteolol
- Glaucoma, Open-Angle
- beta-Arrestins
Cornelissen G, Watanabe Y, Beaty LA, et al.
2025
- Antihypertensive Agents
- Blood Pressure
- Hypertension
A consensus regarding the optimal time to administer anti-hypertensive medications has not been reached. Possible differential effects of different anti-hypertensive drugs on the circadian pattern of blood pressure (BP) and differential responses of individual patients receiving the same treatment at different times of the day may partly account for the controversy. Ambulatory blood pressure monitoring (ABPM) data available at 30-minute intervals for 7 days from previous studies are reanalyzed to compare the effect of five drugs (amlodipine, atenolol, captopril retard, long-acting carteolol, and nilvadipine) taken 1.5 hours after awakening or twice a day on the 24-hour profile of BP from 7 to 13 conventionally diagnosed patients per treatment group. Similar data from 30 patients receiving losartan/hydrochlorothiazide for at least one month at each of six different times in relation to their time of awakening serve to compare the effect of treatment time in different patients. Some but not all drugs affected the 24-hour amplitude and/or phase of BP or the contribution of the 12-hour harmonic term to modify the circadian waveform of BP. While evening dosing increased the 24-hour amplitude of BP in some patients, other patients achieved such a desired effect with morning dosing. Personalized optimization of treatment timing to best match a healthy circadian BP pattern is recommended, guided by chronobiological analyses of ABPM data collected over several days in view of the large day-to-day variability in all features of the 24-hour BP rhythm. • We illustrate how five anti-hypertensive drugs with different mechanisms of action modify patients’ circadian pattern of blood pressure. • We show how different patients respond differently to the same dose of the same anti-hypertensive drug taken at different times of day. • Accordingly, we advocate that chronotherapy of blood pressure be personalized, guided by chronobiological monitoring.
Abstract licence: CC BY
K. Kashiwagi, Kentaro Ouchi, Y. Shibasaki, et al.
Japanese Journal of Ophthalmology, 2023
Chiu CC, Liu KS, Liu CY, et al.
2025
- Adrenergic beta-Antagonists
- Carteolol
- Epinephrine
Ünal E, Yücel MB, Gedikli SN, et al.
2025
- Carteolol
- Hemangioma
- Skin Neoplasms
Lešták Ján, Fůs Martin, Pitrova Sarka
Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia, 2024
- Antihypertensive Agents
- Carteolol
- Glaucoma, Open-Angle
BACKGROUND AND AIM: In a previous follow-up of glaucoma patients taking carteolol or latanoprost, we found a greater progression of visual field changes with the prostaglandin than the betablocker. In the present study we compared the impact of carteolol and latanoprost on peripapillary vessel density in newly diagnosed primary open-angle glaucoma (POAG) patients. METHODS: The study consisted of two groups of POAG patients. There were 46 patient eyes treated with carteolol (Carteol LP 2%) in the first group and 52 eyes treated with latanoprost (Xalatan 0.005%) in the second. Intraocular pressure (IOP), vessel density (VD) and visual field were assessed in all patients. VD was measured peripapillary by optical coherence tomography angiography (OCTA) with the Avanti RTVue XR in eight segments: Inferior Temporal - IT (1); Temporal Inferior -TI (2); Temporal Superior - TS (3); Superior Temporal - ST (4); Superior Nasal - SN (5); Nasal Superior - NS (6); Nasal Inferior - NI (7) and Inferior Nasal - IN (8). The measurements were compared before and after three months of treatment. The visual field was examined with a fast threshold glaucoma program using a Medmont M 700 instrument from Medmont International Pty Ltd. and only when a diagnosis of POAG was done. The overall defect (OD) was assessed. RESULTS: Before treatment, there was no difference between groups in either OD or VD. After treatment, there was a decrease in IOP in both groups. In the carteolol-treated group, the mean decrease was 5.8 mmHg and in the latanoprost-treated eyes, the mean decrease was 7 mmHg. The difference was not statistically significant (P=0.133). After treatment with carteolol, there was a statistically significant increase in VD in segments 4, 5 and 6. After latanoprost treatment, VD was statistically significantly improved only in segment 5. A greater increase in VD values was found in eyes treated with carteolol than in eyes treated with latanoprost. CONCLUSION: Carteolol had a better effect on vessel density than latanoprost.
Abstract licence: CC BY
K. Yoshioka, Tatsuya Kawasaki
Cureus, 2025
Ophthalmic beta-blocker carteolol can rarely cause cardiovascular effects such as bradycardia, heart block, and hypotension. We report a case of carteolol eye drops induced atrioventricular (AV) block. A 76-year-old man with type 2 diabetes developed exercise-induced second-degree AV block, which improved after discontinuing carteolol eye drops in the unilateral eye. Six months later, third-degree AV block recurred due to inadvertent reuse of carteolol eye drops in bilateral eyes despite its prohibition. A seven-day patch electrocardiogram (ECG) monitor showed AV conduction returned to a 1:1 ratio after discontinuation of eye drops. The pacemaker implantation was deferred, and he is currently under close follow-up. Depending on the amount administered to a unilateral eye or bilateral eyes, topical carteolol eye drops can cause second- or third-degree AV block.
Abstract licence: CC BY
Qin Xiang, Jing Yang, Qing Liu, et al.
Scientific Reports, 2025
- Atropine
- Carteolol
- Myopia
Myopia is the most widespread refractive error caused by an increase in the axial length (AL) of the eyeball, and is also a major risk factor for other blinding eye diseases, seriously endangering human health and quality of life. Investigating practical methods to control the progression of myopia is therefore crucial. The only medication that has been shown to effectively delay the progression of myopia over an extended period of time is atropine. Although they have more adverse effects, atropine eye drops with a high concentration work best to correct myopia. Atropine at low concentrations can slow the progression of myopia, however the results might not be very noticeable. It is of great significance to explore the application of drugs to suppress myopia in combination with low-concentration atropine in the treatment of myopia. This study investigated the role and mechanism of 0.01% atropine combined with carteolol hydrochloride in the treatment of myopia. By establishing a model of form-deprivation myopia in guinea pigs, we examined the protective effect of 0.01% atropine combined with carteolol hydrochloride on myopia in guinea pigs and further explored the mechanism of scleral remodeling mediated by mitochondrial dysfunction. We found that 0.01% atropine combined with carteolol hydrochloride refined mitochondrial dysfunction-induced extracellular matrix degradation by activating the PGC-1α/NRF2/HO-1 signaling pathway, thereby suppressing scleral remodeling and the progression of form-deprivation myopia in guinea pigs. In conclusion, 0.01% atropine combined with carteolol hydrochloride may be an effective strategy for the treatment of myopia.
Abstract licence: CC BY-NC-ND
Y. Hashikawa, Yuki Kato, H. Kaji, et al.
Heliyon, 2023
The objectives of this study were to develop a sustained-release device for carteolol hydrochloride (CH) and investigate any potential difference in the intraocular distribution of this agent between the transscleral administration of the device and treatment with eyedrops. The device was formulated with photocurable resin, poly (ethyleneglycol) dimethacrylate, to fit within the curve of the rabbit eyeball. In vitro study showed that CH was released in a sustained-release manner for 2 weeks. The concentration of CH in the retina, choroid/retinal pigment epithelium, sclera, iris, and aqueous humor was determined by high-performance liquid chromatography. Transscleral administration was able to deliver CH to the posterior segment (i.e., retina and choroid/retinal pigment epithelium) rather than the anterior segment (i.e., aqueous humor), while eyedrops delivered CH only to the anterior segment. Transscleral administration could deliver CH to aqueous humor at half the concentration versus treatment with eyedrops and reduced intraocular pressure (IOP) at 1 day after implantation; however, the IOP-lowering effect was not sustained thereafter. In conclusion, transscleral drug delivery may be a useful method for the reduction of IOP. Notably, the aqueous concentration must be equal to that delivered by the eyedrops, and this approach might be preferable for drug delivery to the posterior segment of the eye.
Abstract licence: CC BY
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
9 found
Half-life
Not available
Mechanism
The primary mechanism of the ocular hypotensive action of carteolol in reducing…
Food interactions
None known
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Metabolism
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 599 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
Involved in the regulation of sleep/wake behaviors PMID:31473062
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC S01ED55
ATC S01ED05
ATC C07AA15
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Carteolol
Additional database identifiers
ChemSpider
2485
BindingDB
50040065
HUGO Gene Nomenclature Committee (HGNC)
HGNC:286
GenAtlas
ADRB2
GeneCards
ADRB2
GenBank Gene Database
Y00106
GenBank Protein Database
29371
Guide to Pharmacology
29
UniProt Accession
ADRB2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:285
GenAtlas
ADRB1
GeneCards
ADRB1
GenBank Gene Database
J03019
GenBank Protein Database
178200
Guide to Pharmacology
28
UniProt Accession
ADRB1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Show earlier publications
Structured knowledge from the free knowledge base
Linked open data from Wikidata (Q546434), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.