Betacarotene 30mg tablets
Requires a prescription from a doctor or prescriber
Beta-carotene, with the molecular formula C40H56, belongs to the group of carotenoids consisting of isoprene units.
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Safety monitoring data
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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.
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Suspected adverse reactions reported for Betacarotene
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1 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
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Supply & safety information
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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
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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. 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: 4 · Randomised trials: 2 · Trials: 5 · 1990–2026
Showing the 50 most relevant studies, sorted by most relevant.
Adèle C. Green, Gail Williams, Rachel Ε. Neale, et al.
The Lancet, 1999
- Carcinoma, Basal Cell
- Basal Cell Carcinoma
- Carcinoma, Squamous Cell
Kotepui KU, Mahittikorn A, Wilairatana P, et al.
2023
Backgroundβ-Carotene, which is a prominent carotenoid with notable antioxidant properties, may play a role in countering the oxidative stresses induced by malaria. The association between β-carotene levels and malaria is not yet fully understood, prompting this systematic review and meta-analysis.MethodsA rigorous search of databases, including Nursing and Allied Health Premium, EMBASE, MEDLINE, Ovid, PubMed, Scopus, and Google Scholar, was undertaken to collate studies that focused on β-carotene levels in malaria patients. The selected studies underwent critical appraisal, followed by data extraction for a meta-analysis.ResultsOf the 2498 records initially identified, 10 were deemed suitable for synthesis. A considerable number of these studies indicated a pronounced reduction in β-carotene levels among malaria patients in contrast with uninfected individuals. The meta-analysis, encompassing 421 malaria patients and 240 uninfected controls, revealed a significant correlation between reduced β-carotene levels and malaria (p 2: 93.86%, seven studies).ConclusionsThe conducted systematic review and meta-analysis corroborated the correlation between lower β-carotene levels and malaria. The intricate relationship between malaria and β-carotene merits deeper exploration. A comprehensive understanding of this association might pave the way for innovative therapeutic approaches leveraging the antioxidant attributes of β-carotene to combat malaria-induced oxidative stress.
Abstract licence: CC BY
Wu LY, Chen JX, Chen GS, et al.
2022
- Parkinson Disease
- beta Carotene
- Ascorbic Acid
BackgroundThe beneficial effects of dietary β-carotene and vitamin A on Parkinson disease (PD) have been confirmed, but some studies have yielded questionable results. Therefore, this meta-analysis investigated the effect of dietary β-carotene and vitamin A on the risk of PD.MethodsThe following databases were searched for relevant paper: PubMed, Embase, Medline, Scopus, Cochrane Library, CNKI, Wanfang Med online, and Weipu databases for the relevant paper from 1990 to March 28, 2022. The studies included were as follows: β-carotene and vitamin A intake was measured using scientifically recognized approaches, such as food frequency questionnaire (FFQ); evaluation of odds ratios using OR, RR, or HR; β-carotene and vitamin A intake for three or more quantitative categories; and PD diagnosed by a neurologist or hospital records.ResultsThis study included 11 studies (four cohort studies, six case-control studies, and one cross-sectional study). The high β-carotene intake was associated with a significantly lower chance of developing PD than low β-carotene intake (pooled OR = 0.83, 95%CI = 0.74-0.94). Whereas the risk of advancement of PD was not significantly distinctive among the highest and lowest vitamin A intake (pooled OR = 1.08, 95%CI = 0.91-1.29).ConclusionsDietary β-carotene intake may have a protective effect against PD, whereas dietary vitamin A does not appear to have the same effect. More relevant studies are needed to include into meta-analysis in the further, as the recall bias and selection bias in retrospective and cross-sectional studies cause misclassifications in the assessment of nutrient intake.
Abstract licence: CC BY-NC
Yi Zhang, Yi Zhang, Jun Ding, et al.
Frontiers in Nutrition, 2022
Gilbert S. Omenn, Gary E. Goodman, Mark Thornquist, et al.
JNCI Journal of the National Cancer Institute, 1996
- Retinyl Esters
- Antioxidants
- Asbestos
Schulze Kerry, Massie Allan, Shamim Abu, et al.
Trials, 2011
S. T. Mayne, Garry J. Handelman, Gary R. Beecher
JNCI Journal of the National Cancer Institute, 1996
- Antioxidants
- Clinical Trials as Topic
- Lung Neoplasms
Joyce Van Eck, Brian Conlin, David F. Garvin, et al.
American Journal of Potato Research, 2007
M. Daviglus, A. Dyer, V. Persky, et al.
Epidemiology, 1996
Sarker U, Oba S, Daramy MA
2020
- Amaranthus
- Plant Leaves
- Minerals
We evaluated 17 genotypes of stem amaranth (Amaranthus lividus) in terms of dietary fiber, moisture, carbohydrates, fat, ash, gross energy, protein, minerals, phytopigments, total antioxidant capacity (TAC), vitamins, total flavonoids (TFC), total polyphenols (TPC) and their variations. Stem amaranth leaves have abundant dietary fiber, moisture, carbohydrates, and protein. We found significant amount of potassium, calcium, magnesium (9.61, 24.40, and 29.77 mg g-1 DW), iron, manganese, copper, zinc, (1131.98, 269.89, 25.03, and 1006.53 µg g-1 DW), phytopigments such as chlorophyll a, chlorophyll ab chlorophyll b, (27.76, 42.06, and 14.30 mg 100 g-1 FW), betalain, betaxanthin, betacyanin (62.92, 31.81, 31.12 µg 100 g-1 FW), total carotenoids, beta-carotene (1675.38, 1289.26 µg g-1 FW), vitamin C (1355.46 µg g-1 FW), TPC, TFC (228.63 GAE and 157.42 RE µg g-1 DW), and TAC (DPPH, ABTS+) (26.61, 51.73 TEAC µg g-1 DW) in the leaves of stem amaranth. Genotypes exhibited a wide range of variations. Three genotypes DS40, DS30, and DS26 could be used as an antioxidant profile enriched stem amaranth. Phenolics, phytopigments, flavonoids, and vitamins of stem amaranth leaves exhibited strong antioxidant activity. Stem amaranth could be a potential source of dietary fiber, moisture, carbohydrates, protein, minerals, phenolics, phytopigments, flavonoids, and vitamins in our daily diet for attaining nutritional and antioxidant sufficiency.
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
None known
Half-life
6-11 days
Mechanism
Beta-carotene is an antioxidant that presents significant efficacy against the reactive oxygen species singlet oxygen.
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
6-7 hours
Half-life
6-11 days
[A32487]
Protein binding
Volume of distribution
Metabolism
Elimination
[L2202]
It is also excreted in feces and urine as metabolites.
[L2214]…
Clearance
[A32488]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L2191]
It is also approved to be used as a color additive for food products,[L2192] drugs (with the label of "only as a color additive")[L2193] and cosmetics.
[L2194]
It is used commonly for the reduction of photosensitivity in patients with erythropoietic protoporphyria and other photosensitivity diseases.
[A32485]
Known interactions with other medications. Always consult a healthcare professional.
Showing 1 of 1 interactions
[L2202]
The registered LD50 of beta-carotene is >5000 mg/kg.MSDS
The effect of beta-carotene in the immune response is thought to be related to the direct effect on the thymus which increases the production of immune cells.[L2202]
Other than the antioxidant activities, some other actions have been correlated to beta-carotene. It is thought to have detoxifying properties, as well as to help increase resistance to inflammation and infection and increase immune response and enhance RNA production.[L2202]
How the body processes this drug — absorption, distribution, metabolism, and elimination
The absorption of beta-carotene is thought to be performed in 6-7 hours.
[L2202]
The reported AUC of beta-carotene when administered orally from 0 to 440 hours after initial administration was reported to be 26.3 mcg.h/L. The maximal concentration of beta-carotene is attained in a dual pharmacokinetic profile after 6 hours and again after 32 hours with a concentration of 0.58 micromol/L.
[A32488]
[A32487]
[L2202]
[L2202]
It is also excreted in feces and urine as metabolites.
[L2214]
The consumption of dietary fiber can increase the fecal excretion of fats and other fat-soluble compounds such as beta-carotene.
[L2226]
[A32488]
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that carry this drug through the body
PMID:24381170 PMID:30873003
In the off-state of the pathway, forms homooligomers or heterooligomers with LRP8 .
PMID:30873003
Upon binding to ligands, homooligomers are rearranged to higher order receptor clusters that transmit the extracellular RELN signal to intracellular signaling processes by binding to DAB1 .
PMID:30873003
This interaction results in phosphorylation of DAB1 leading to the ultimate cell responses required for the correct positioning of newly generated neurons. Later, mediates a stop signal for migrating neurons, preventing them from entering the marginal zone (By similarity)
PMID:22665496 PMID:26900151 PMID:28057518
Accepts retinol from the transport protein STRA6, and thereby contributes to retinol uptake, storage and retinoid homeostasis PMID:15632377 PMID:22665496
PMID:5541771
Delivers retinol from the liver stores to the peripheral tissues (Probable). Transfers the bound all-trans retinol to STRA6, that then facilitates retinol transport across the cell membrane PMID:22665496
ATC A11CA02
ATC D02BB01
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)
Beta carotene
Matched from: Betacarotene
Additional database identifiers
Drugs Product Database (DPD)
11079
Drugs Product Database (DPD)
704
ChemSpider
4444129
BindingDB
54988
PDB
BCR
ZINC
ZINC000006845076
HUGO Gene Nomenclature Committee (HGNC)
HGNC:13815
GeneCards
BCO1
UniProt Accession
BCDO1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12698
GeneCards
VLDLR
GenBank Gene Database
L20470
GenBank Protein Database
409426
UniProt Accession
VLDLR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9919
GenAtlas
RBP1
GeneCards
RBP1
GenBank Gene Database
M11433
GenBank Protein Database
190948
UniProt Accession
RET1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9920
GenAtlas
RBP2
GeneCards
RBP2
GenBank Gene Database
U13831
GenBank Protein Database
535390
UniProt Accession
RET2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9921
GenAtlas
RBP3
GeneCards
RBP3
GenBank Gene Database
M33875
GenBank Protein Database
186541
UniProt Accession
RET3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9922
GenAtlas
RBP4
GeneCards
RBP4
GenBank Gene Database
X00129
GenBank Protein Database
35897
Guide to Pharmacology
2549
UniProt Accession
RET4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:15847
GenAtlas
RBP5
GeneCards
RBP5
GenBank Gene Database
AY007436
GenBank Protein Database
13447447
UniProt Accession
RET5_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
Linked open data from Wikidata (Q306135), 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.