Dexamethasone 0.1% / Neomycin 0.5% / Acetic acid (glacial) 2% ear spray
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8 branded products available
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Otomize ear spray
Dexamethasone 0.1% / Neomycin 0.5% / Acetic acid (glacial) 2% ear spray
Dexamethasone 0.1% / Neomycin 0.5% / Acetic acid (glacial) 2% ear spray
Dexamethasone 0.1% / Neomycin 0.5% / Acetic acid (glacial) 2% ear spray
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. 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.
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. 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: 1 · Randomised trials: 3 · 1990–2025
Showing the 50 most relevant studies, sorted by most relevant.
Zhao S, Jang C, Liu J, et al.
2020
- Lipogenesis
- Liver
- Hepatocytes
Consumption of fructose has risen markedly in recent decades owing to the use of sucrose and high-fructose corn syrup in beverages and processed foods1, and this has contributed to increasing rates of obesity and non-alcoholic fatty liver disease2-4. Fructose intake triggers de novo lipogenesis in the liver4-6, in which carbon precursors of acetyl-CoA are converted into fatty acids. The ATP citrate lyase (ACLY) enzyme cleaves cytosolic citrate to generate acetyl-CoA, and is upregulated after consumption of carbohydrates7. Clinical trials are currently pursuing the inhibition of ACLY as a treatment for metabolic diseases8. However, the route from dietary fructose to hepatic acetyl-CoA and lipids remains unknown. Here, using in vivo isotope tracing, we show that liver-specific deletion of Acly in mice is unable to suppress fructose-induced lipogenesis. Dietary fructose is converted to acetate by the gut microbiota9, and this supplies lipogenic acetyl-CoA independently of ACLY10. Depletion of the microbiota or silencing of hepatic ACSS2, which generates acetyl-CoA from acetate, potently suppresses the conversion of bolus fructose into hepatic acetyl-CoA and fatty acids. When fructose is consumed more gradually to facilitate its absorption in the small intestine, both citrate cleavage in hepatocytes and microorganism-derived acetate contribute to lipogenesis. By contrast, the lipogenic transcriptional program is activated in response to fructose in a manner that is independent of acetyl-CoA metabolism. These data reveal a two-pronged mechanism that regulates hepatic lipogenesis, in which fructolysis within hepatocytes provides a signal to promote the expression of lipogenic genes, and the generation of microbial acetate feeds lipogenic pools of acetyl-CoA.
Abstract licence: CC BY
H. Osborne, G. Allison
British Journal of Sports Medicine, 2006
P. Zalewski, I. J. Forbes, W. Betts
The Biochemical journal, 1993
Akin Delbarre, Philippe Muller, Viviane Imhoff, et al.
Planta, 1996
Amani S, Moeini M
2016
Balogun FO, Ajao AA, Sabiu S
2023
Daniellia oliveri has found its indigenous relevance in the management of diseases including but not limited to diabetes mellitus, tuberculosis, fever, ulcers, pain, worm manifestation, pneumonia, skin ailments, infectious diseases, sickle cell anaemia, hence, a review of its indigenous knowledge, ethnopharmacological and nutritional benefits was undertaken. Information used for the review was sourced from popular scientific databases (Google Scholar, PubMed, Science Direct, Web of Science, BioMed Central, JSTOR, African Plant, Global Biodiversity Information and others), conference proceedings, dissertations or theses, chapters in books, edited books, and journal collections. The materials obtained from 121 scientific documents targeting majorly between 1994 and 2023 established the presence of major secondary metabolites (such as polyphenols, flavonoids, saponins, alkaloids, etc.), minerals (e.g., sodium, potassium, phosphorus, selenium, calcium, magnesium, etc.), vitamins (beta-carotene, thiamine, riboflavin, niacin, ascorbic acid, etc.), and nutrients (crude protein, moisture, dry matter, ether, carbohydrates, and energy). Literature also lent credence to the preliminary safety profiles of the plant and its pharmacological potentials as analgesic, antinociceptive, antioxidant, antidiabetic, antidiarrhoeal, anthelmintic, anti-inflammatory, antimelanogenesis, antimicrobial, antiplasmodial, antisickling, cardiotoxic, cytotoxic, and neuroprotective agents. While the review is majorly limited to Africa particularly western countries (such as Nigeria, Burkina Faso, Mali, Ghana, Togo, and Benin) and the plant is found to be largely underutilized, it is evident that limited information exists on the in vivo pharmacological evaluation, bioactive compounds identification, and there is a lack of preclinical and clinical trials for possible drug development. Based on the aforementioned, it is hoped that further research studies geared toward providing insights into the established grey areas (such as traditional use investigation, targeted or assay-guided compounds identification, and preclinical and clinical studies) are necessary in order to fully explore the therapeutic, nutritional, and economic benefits of the plant.
Abstract licence: CC BY-NC-ND
M. N. Johnston, E. Flook, D. Mehta, et al.
Clinical Otolaryngology, 2006
- Otitis Externa
- Mastoiditis
- Acute Disease
L. B. Rodrigues, H. F. Leite, M. Yoshida, et al.
International journal of pharmaceutics, 2009
K. Y. Kareem, T. Loh, H. Foo, et al.
Poultry Science, 2016
Mahsa Ekhtiar, Maryam Ghasemi-Dehnoo, Yousef Mirzaei, et al.
International immunopharmacology, 2023
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.
Scientific data (pharmacology, interactions, ADME) is not yet available for this medicine. Clinical sections are sourced from the NHS dm+d database.