Phytomenadione 500micrograms/5ml oral suspension
Requires a prescription from a doctor or prescriber
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1 branded products available
Part of the Konakion brand family (generic: Phytomenadione)
MHRA licensed products
View all licensed products for Phytomenadione on the MHRA register
WHO defined daily dose (DDD)
20 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 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.
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Codes for healthcare professionals and prescribing systems
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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: 6 · Randomised trials: 1 · Trials: 18 · 1988–2026
Showing the 50 most relevant studies, sorted by most relevant.
Simionescu AA, Danciu BM, Stanescu AMA
2021
Anaphylactic reactions during pregnancy can range from subjective cutaneous symptoms to anaphylaxis and lethal anaphylactic shock. The fetal and maternal outcomes are unpredictable. This study is the first systematic review of the clinical presentation of severe anaphylaxis in pregnancy as defined by the World Allergy Organization to determine maternal and fetal outcomes. We searched PubMed, the Web of Science, and Scopus databases for articles published between 1 January 1985 and 15 April 2021 using the following terms (((anaphylactic shock) AND (pregnancy)) OR ((anaphylaxis) AND (pregnancy))). In 42 studies involving 47 patients, 36.17% of patients were 31-35 years old, and 74.47% of cases occurred peripartum, mostly during cesarean section. Accurate diagnosis with valid and reliable outcome measures was reported for 71.74% of cases. Twenty-two allergens were identified: antibiotics (penicillins and cephalosporins), anesthetic drugs (suxamethonium, mepivacaine), latex, oxytocin, sodium and sucrose iron, laminaria, misoprostol, rubber from Foley catheter, oral phytomenadione, ranitidine, chamomile, and ant sting. Two cases of maternal death related to latex and intravenous iron sucrose, and six infants with neurological disease were reported, mostly related to antibiotics. This review of the currently available literature shows that favorable outcomes are attainable with a high degree of observation, multidisciplinary cooperation, and rapid treatment.
Abstract licence: CC BY
Sapapsap B, Srisawat C, Suthumpoung P, et al.
2022
- Thromboembolism
- Blood Coagulation Disorders
- Heart Valves
BackgroundPatients who had mechanical heart valves and an international normalized ratio (INR) of >5.0 should be managed by temporary cessation of vitamin K antagonist. This study aimed to investigate the safety of low-dose vitamin K1 in patients with mechanical heart valves who have supratherapeutic INR.MethodsCINAHL, Cochran Library, Clinical trial.gov, OpenGrey, PubMed, ScienceDirect, and Scopus were systematically searched from the inception up to October 2021 without language restriction. Studies comparing the safety of low-dose vitamin K1 treatment in patients with placebo or other anticoagulant reversal agents were included. We used a random-effect model for the meta-analysis. Publication bias was determined by a funnel plot with subsequent Begg's test and Egger's test.ResultsFrom 7529 retrieved studies, 3 randomized control trials were included in the meta-analysis. Pooled data demonstrated that low-dose vitamin K was not associated with thromboembolism rate (risk ratio [RR] = 0.94; 95% CI: 0.19-4.55) major bleeding rate (RR = 0.58; 95% CI: 0.07-4.82), and minor bleeding rate (RR = 0.60; 95% CI: 0.07-5.09). Subgroup and sensitivity analysis demonstrated the nonsignificant effect of low-dose vitamin K on the risk of thromboembolism. Publication bias was not apparent, according to Begg's test and Egger's test (P = .090 and 0.134, respectively).ConclusionThe current evidence does not support the role of low-dose vitamin K as a trigger of thromboembolism in supratherapeutic INR patients with mechanical heart valves. Nevertheless, more well-designed studies with larger sample sizes are required to justify this research question.
Abstract licence: CC BY-NC
Simes DC, Viegas CSB, Araújo N, et al.
2020
- Dietary Supplements
- Vitamin K
- Vitamin K 1
Vitamin K health benefits have been recently widely shown to extend beyond blood homeostasis and implicated in chronic low-grade inflammatory diseases such as cardiovascular disease, osteoarthritis, dementia, cognitive impairment, mobility disability, and frailty. Novel and more efficient nutritional and therapeutic options are urgently needed to lower the burden and the associated health care costs of these age-related diseases. Naturally occurring vitamin K comprise the phylloquinone (vitamin K1), and a series of menaquinones broadly designated as vitamin K2 that differ in source, absorption rates, tissue distribution, bioavailability, and target activity. Although vitamin K1 and K2 sources are mainly dietary, consumer preference for diet supplements is growing, especially when derived from marine resources. The aim of this review is to update the reader regarding the specific contribution and effect of each K1 and K2 vitamers in human health, identify potential methods for its sustainable and cost-efficient production, and novel natural sources of vitamin K and formulations to improve absorption and bioavailability. This new information will contribute to foster the use of vitamin K as a health-promoting supplement, which meets the increasing consumer demand. Simultaneously, relevant information on the clinical context and direct health consequences of vitamin K deficiency focusing in aging and age-related diseases will be discussed.
Abstract licence: CC BY
Rachel B. Britt, Jamie N. Brown
Clinical and Applied Thrombosis/Hemostasis, 2018
- Drug Hypersensitivity
- Anaphylaxis
- Vitamin K 1
Chawla D, Deorari AK, Saxena R, et al.
2007
- Vitamin K Deficiency
- Vitamin K 1
- Vitamin K 3
Miao Zhang, Jing Chen, Chun-xiao Wang, et al.
World Journal of Clinical Cases, 2022
Lutfi LL, Shaaban MI, Elshaer SL
2024
- Biofilms
- Gram-Negative Bacteria
- Vitamin K 1
BackgroundThe persistent surge in antimicrobial resistance represents a global disaster. The initial attachment and maturation of microbial biofilms are intimately related to antimicrobial resistance, which in turn exacerbates the challenge of eradicating bacterial infections. Consequently, there is a pressing need for novel therapies to be employed either independently or as adjuvants to diminish bacterial virulence and pathogenicity. In this context, we propose a novel approach focusing on vitamin D and vitamin K1 as potential antibiofilm agents that target Gram-negative bacteria which are hazardous to human health.ResultsOut of 130 Gram-negative bacterial isolates, 117 were confirmed to be A. baumannii (21 isolates, 17.9%), K. pneumoniae (40 isolates, 34.2%) and P. aeruginosa (56 isolates, 47.9%). The majority of the isolates were obtained from blood and wound specimens (27.4% each). Most of the isolates exhibited high resistance rates to β-lactams (60.7-100%), ciprofloxacin (62.5-100%), amikacin (53.6-76.2%) and gentamicin (65-71.4%). Approximately 93.2% of the isolates were biofilm producers, with 6.8% categorized as weak, 42.7% as moderate, and 50.4% as strong biofilm producers. The minimum inhibitory concentrations (MICs) of vitamin D and vitamin K1 were 625-1250 µg mL-1 and 2500-5000 µg mL-1, respectively, against A. baumannii (A5, A20 and A21), K. pneumoniae (K25, K27 and K28), and P. aeruginosa (P8, P16, P24 and P27) clinical isolates and standard strains A. baumannii (ATCC 19606 and ATCC 17978), K. pneumoniae (ATCC 51503) and P. aeruginosa PAO1 and PAO14. Both vitamins significantly decreased bacterial attachment and significantly eradicated mature biofilms developed by the selected standard and clinical Gram-negative isolates. The anti-biofilm effects of both supplements were confirmed by a notable decrease in the relative expression of the biofilm-encoding genes cusD, bssS and pelA in A. baumannii A5, K. pneumoniae K28 and P. aeruginosa P16, respectively.ConclusionThis study highlights the anti-biofilm activity of vitamins D and K1 against the tested Gram-negative strains, which emphasizes the potential of these vitamins for use as adjuvant therapies to increase the efficacy of treatment for infections caused by multidrug-resistant (MDR) strains and biofilm-forming phenotypes. However, further validation through in vivo studies is needed to confirm these promising results.
Abstract licence: CC BY
R. von Kries
Drug safety, 1999
G Agostini, ET Mooney, ELW Wilkie, et al.
Australian Veterinary Journal, 2025
- Cat Diseases
- Dog Diseases
- Vitamin K 1
Miyazawa S, Uesawa Y
2026
Background: /Objective: Vitamin K (VK) comprises a family of quinone compounds with potential involvement in cell death-related pathways through their redox properties. However, consistent findings have not been obtained regarding the clinical significance of VK in breast cancer (BC). Thus, we used the FDA Adverse Event Reporting System (FAERS) to examine the co-reporting patterns of BC-related adverse-event terms among VK-related reports. Methods: Reporting disproportionality analysis was conducted using FAERS data spanning the first quarter of 2004 to the third quarter of 2024. BC-related reports were defined using all valid Preferred Terms included in the relevant narrow-scope Standardized MedDRA Query (SMQ). Reporting odds ratios (RORs) and proportional reporting ratios were calculated for all VK types and each homolog, followed by exploratory comparisons with other compounds containing quinone structures. Results: In total, 32,156 VK-related reports were identified, including 136 BC-related reports. VK-related reports showed significantly lower reporting disproportionality for breast cancer-related reports (ROR = 0.486, 95% confidence interval = 0.411–0.575). In homolog-specific analyses, similar trends were observed for the quinone-type homologs phytomenadione, menatetrenone, and menadione, whereas no significant reporting disproportionality was detected for the hydroquinone-type homolog menadiol. Conclusions: The differences in reporting patterns among quinone-type VK homologs, hydroquinone-type VK, and other quinone-containing compounds suggest that differences in redox properties may be partially related to the structure of reporting disproportionality. Although this study did not demonstrate causality or clinical efficacy, it provides a hypothesis-generating basis for linking basic, epidemiological, and clinical research using FAERS data. Future validation through mechanistic research and analytical epidemiological studies with stricter control of confounding is warranted.
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
22 minutes
Mechanism
Vitamin K is a cofactor of gamma-carboxylase.
Food interactions
None known
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
4 µg
Half-life
22 minutes
[A234104]
Volume of distribution
6 L
[A234374]
Metabolism
[A137578]
…
Elimination
36%
[A234104][A234329]
Clearance
90%
[A234104][A234329]
…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Phylloquinone has been synthesized since at least 1939,[A234384] and was approved by the FDA prior to 1955.[L33389]
[L33345]
Parenteral (intravenous, intramuscular, and subcutaneous) phylloquinone is indicated to treat coagulation disorders due to faulty formation of coagulation factors II, VII, IX, and X caused by vitamin K deficiency or some interference with vitamin K activity.
[L33319]
These indications include the above indications as well as hypoprothrombinemia secondary to sprue, ulcerative colitis, celiac disease, intestinal resection, pancreatic cystic fibrosis, or regional enteritis; or hypoprothrombinemia caused by interference with vitamin k metabolism.
[L33319]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 739 interactions
[A234259]
Intravenous administration has been associated with an increased risk of toxicity.
[A234284]
These patients should be treated with symptomatic and supportive measures.
The intravenous LD50 in mice is 1170 mg/kg and the oral LD50 is >24180 mg/kg.
[L33345]
Vitamin K may also carboxylate matrix proteins in chondrocytes, inhibiting calcification of joints, and may increase type II collagen.[A234304] The role of vitamin K in osteroarthritis,[A234304] bone density,[A234309] and vascular calcification[A234314] is currently under investigation.
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A234264]
1.5 ± 0.8 nmol is found in the plasma compartment, and 3.6 ± 3.4 nmol is found in the second compartment.
[A234264]
A 10 mg intramuscular phylloquinone dose is 89.2% ± 25.4% bioavailable.
[A234344]
The same dose reaches a mean Cmax of 67 ± 30 ng/mL, with a mean Tmax of 9.2 ± 6.6 hours, and an AUC of 1700 ± 500 h\*ng/mL.
[A234344]
A 10 mg intravenous phylloquinone dose has a mean AUC of 1950 ± 450 h\*ng/mL.
[A234344]
[A234104]
[A234374]
[A137578]
The side chain is then cleaved to 5 or 7 carbons long, and then glucuronidated prior to elimination.
[A234104][A234109][A234114][A234119]
Vitamin Ks in general undergo a cycle of reduction to vitamin K hydroquinone by vitamin K epoxide reductase (VKOR), oxidation to vitamin K epoxide by gamma-glutamyl carboxylase, and converted back to vitamin K by VKOR.
[A234259]
[A234104][A234329]
[A234104][A234329]
A 10 mg intravenous dose of phylloquinone has a mean clearance of 91 ± 24 mL/min.
[A234344]
Proteins and enzymes this drug interacts with in the body
PMID:17073445
Catalyzes gamma-carboxylation of various proteins, such as blood coagulation factors (F2, F7, F9 and F10), osteocalcin (BGLAP) or matrix Gla protein (MGP) PMID:17073445
PMID:2019570 PMID:21976677
Triggers the production of pro-inflammatory cytokines, such as MCP-1/CCL2 and IL8/CXCL8, in endothelial cells PMID:30568593 PMID:9780208
PMID:3019668 PMID:6967872
Functions to limit bone formation without impairing bone resorption or mineralization (By similarity). It binds strongly to apatite and calcium PMID:6967872
Enzymes involved in drug metabolism — important for understanding drug interactions
Involved compounds
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ATC B02BA01
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)
Phylloquinone
Matched from: Phytomenadione
Additional database identifiers
Drugs Product Database (DPD)
4918
ChemSpider
4447652
BindingDB
24782
PDB
PQN
ZINC
ZINC000003831332
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4247
GenAtlas
GGCX
GeneCards
GGCX
GenBank Gene Database
M81592
GenBank Protein Database
184028
UniProt Accession
VKGC_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3535
GenAtlas
F2
GeneCards
F2
GenBank Gene Database
M17262
GenBank Protein Database
339641
Guide to Pharmacology
2362
UniProt Accession
THRB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1043
GenAtlas
BGLAP
GeneCards
BGLAP
GenBank Gene Database
X53698
GenBank Protein Database
36093
UniProt Accession
OSTCN_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2645
GeneCards
CYP4F2
Guide to Pharmacology
1344
UniProt Accession
CP4F2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:30791
GeneCards
UBIAD1
UniProt Accession
UBIA1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:23663
GenAtlas
VKORC1
GeneCards
VKORC1
GenBank Gene Database
AY423044
GenBank Protein Database
40217983
Guide to Pharmacology
2645
UniProt Accession
VKOR1_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72