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Vitamin K2 (VK2) has emerged as a promising agent in cancer therapy, demonstrating anti-cancer effects across a variety of malignancies, including liver, leukaemia, ovarian, pancreatic, breast, and bladder cancers157. Its mechanisms of action are multi-faceted, targeting cancer cell growth and survival through several biological pathways.
Cell-Cycle Arrest and Differentiation
VK2 can inhibit the proliferation of cancer cells by inducing cell-cycle arrest, particularly at the G1 phase, thereby preventing cancer cells from progressing through their growth cycle16. It also promotes the differentiation of malignant cells, making them less aggressive and more susceptible to therapeutic interventions7.
Induction of Apoptosis and Autophagy
VK2 triggers programmed cell death (apoptosis) and autophagy in cancer cells. For example, in bladder cancer, VK2 induces metabolic stress, activating the AMPK pathway and suppressing mTORC1, which leads to autophagic cell death3. This process is further enhanced under glucose-limited conditions, suggesting VK2 may exploit metabolic vulnerabilities unique to cancer cells3.
Suppression of Tumour Invasion
In vitro studies have shown that VK2 can suppress the invasion and metastatic potential of various cancer cell lines, further limiting tumour progression1.
Modulation of Key Metabolic Pathways
VK2 influences cancer cell metabolism, notably by promoting glycolysis while suppressing the TCA cycle in bladder cancer cells. This metabolic shift can induce cellular stress and death in tumours reliant on altered energy production pathways3.
Antioxidant and Anti-Apoptotic Effects
VK2 exhibits antioxidant properties, reducing reactive oxygen species (ROS) and protecting cells from oxidative damage. In neuronal models, VK2 pre-treatment reduced apoptosis and increased glutathione levels, suggesting a broader cytoprotective role that may also be relevant in cancer contexts2.
Clinical Case Reports and Trials
Several case reports highlight VK2’s clinical potential. For instance, VK2 administration led to remission in patients with myelodysplastic syndrome and acute promyelocytic leukaemia, especially when combined with other agents like retinoic acid17. In liver cancer, VK2 supplementation has been associated with reduced recurrence rates and improved prognosis after surgical treatment47.
Animal Studies
In animal models, VK2 significantly inhibited tumour growth in hepatocellular carcinoma (HCC) and colorectal cancer without notable toxicity15. VK2-treated mice displayed reduced tumour sizes and improved survival rates, supporting its safety and efficacy profile35.
VK2 may enhance the efficacy of conventional chemotherapeutics while reducing their side effects. Combination treatments have shown additive or synergistic effects in both preclinical and clinical settings, making VK2 a valuable adjunct in cancer management16.
VK2 is generally well-tolerated, with minimal toxicity observed in both clinical and animal studies, further supporting its use as a therapeutic or preventive agent in oncology15.
| Mechanism | Evidence Type | Cancer Types Studied | Key Findings |
|---|---|---|---|
| Cell-cycle arrest | In vitro, animal | HCC, leukaemia, ovarian, others | Inhibits proliferation, induces differentiation |
| Apoptosis & autophagy | In vitro, animal | Bladder, liver, leukaemia, ovarian | Triggers cell death, especially under metabolic stress |
| Metabolic pathway modulation | In vitro, animal | Bladder | Promotes glycolysis, induces metabolic stress |
| Suppression of invasion | In vitro | Multiple | Reduces metastatic potential |
| Clinical outcomes | Case reports, trials | HCC, leukaemia, myelodysplastic synd. | Reduced recurrence, remission, improved prognosis |
| Combination therapy | Clinical, preclinical | Multiple | Enhanced efficacy, reduced side effects |
Vitamin K2 demonstrates significant anti-cancer properties through multiple mechanisms, including cell-cycle arrest, induction of apoptosis and autophagy, metabolic modulation, and suppression of tumour invasion. Clinical and preclinical evidence supports its potential as both a standalone and adjunctive therapy in various cancers, with a strong safety profile and minimal toxicity13567. Further research and well-designed clinical trials are warranted to fully elucidate its therapeutic potential and optimal application in cancer care.
A recommended safe dosage for vitamin K2 has not been officially established as a maximum limit, but current evidence indicates that it is well tolerated and safe across a broad range of doses. For general health, the typical adequate intake (AI) for vitamin K (all forms) is 120 micrograms (mcg) per day for adult men and 90 mcg per day for adult women, including those who are pregnant or breastfeeding158.
For vitamin K2 specifically, most supplement products and studies use doses in the range of 50–180 mcg per day for the MK-7 subtype, with some research using up to 360 mcg per day for cardiovascular benefits578. In Japan and some clinical studies, much higher doses of the MK-4 subtype (up to 45 milligrams, or 45,000 mcg per day) have been used safely, particularly for bone health and certain medical conditions4789.
No upper tolerable intake level (UL) has been set for vitamin K2, as there is no evidence of toxicity from high oral doses in healthy individuals58. Doses up to 45 mg per day have been administered for up to two years without reports of harm5. The most commonly reported side effects are mild gastrointestinal symptoms, such as nausea or diarrhoea, and these are rare5.
However, vitamin K2 can interact with anticoagulant medications such as warfarin, potentially affecting blood clotting. Individuals on these medications should only take vitamin K2 under medical supervision589.
| K2 Subtype | Common Daily Dosage | High Dose in Studies | Safety/Toxicity Evidence |
|---|---|---|---|
| MK-7 | 50–180 mcg | Up to 360 mcg | No toxicity reported |
| MK-4 | 1–45 mg (1,000–45,000 mcg) | Up to 45 mg | No toxicity reported |
In summary, vitamin K2 is considered safe at both standard and high supplemental doses, with no established toxicity in healthy adults. For most people, a daily dose of 100–180 mcg (MK-7) is typical, while much higher doses (up to 45 mg MK-4) are used in some clinical settings. Always consult a healthcare provider before starting high-dose supplementation, especially if you are taking blood-thinning medication56789.
Bile Duct Cancer, Breast Cancer, Colorectal Cancer, Leukemia, Liver Cancer, Lung Cancer, Ovarian Cancer, Pancreatic Cancer, Stomach Cancer
Multiple clinical studies and case reports investigating vitamin K2 (VK2) as an anti-cancer agent—using doses up to and exceeding 40 mg per day—have found VK2 to be remarkably safe. Notably, no significant side effects were reported, even at these high therapeutic doses used in cancer therapy523.
Specifically, studies in patients with leukaemia, liver cancer, and ovarian cancer have documented the absence of adverse effects, including those related to blood clotting, even at daily doses of 45 mg (MK-4 subtype), which are much higher than typical nutritional intakes52.
In a large, randomised, controlled trial in hepatocellular carcinoma (HCC) patients, vitamin K2 at both 45 mg and 90 mg daily did not increase the incidence of adverse effects compared to placebo23.
| Dose Range (per day) | Cancer Types Studied | Reported Side Effects | Notes |
|---|---|---|---|
| Up to 40 mg (MK-4) | Ovarian, leukaemia, liver | None observed | No hypercoagulability or other adverse effects, even at high doses5 |
| 45–90 mg (MK-4) | Liver (HCC, post-surgery) | None observed | No increase in adverse effects vs placebo in large RCTs23 |
No side effects from vitamin K2 therapy were observed in any clinical studies, even at doses exceeding 40 mg per day5.
There were no reports of hypercoagulable states or other significant adverse reactions, supporting the excellent safety profile of VK2, even at therapeutic doses for cancer52.
This safety profile contrasts with vitamin K3 (menadione), which is known to be toxic at high doses, while K2 is not3.
Some sources suggest that the only notable risk is for individuals taking anticoagulant medications (such as warfarin), as vitamin K2 can interfere with these drugs’ effects on blood clotting. Such individuals should only use VK2 under medical supervision.
Vitamin K2, even at high therapeutic doses used in cancer treatment (up to 90 mg per day), is consistently reported to be well tolerated and free from significant side effects in both clinical and research settings523. This makes VK2 a promising adjunct or alternative in cancer therapy, with an excellent safety margin for most patients.
Vitamin K2 (VK2) has been extensively tested in combination with conventional cancer therapies, demonstrating synergistic effects, enhanced efficacy, and reduced toxicity across multiple cancer types. Below is a detailed overview of key findings:
Sorafenib:
Combining VK2 with the multikinase inhibitor sorafenib synergistically inhibits HCC growth in vitro and in vivo. Pretreatment with VK2 enhances sorafenib’s ability to induce cell-cycle arrest (G0/G1 phase) and apoptosis, while reducing sorafenib-induced side effects. Animal studies showed significant tumour suppression in xenograft models, with no additional toxicity156.
5-Fluorouracil (5-FU):
VK2 augments 5-FU’s growth-inhibitory effects by suppressing NF-κB activation and cyclin D1 expression, leading to G1 cell-cycle arrest. This combination improves therapeutic outcomes in HCC cells without the toxicity typical of other 5-FU-based regimens6.
1,25(OH)₂D₃ (Vitamin D):
VK2 enhances the tumour-suppressive effects of vitamin D in triple-negative breast cancer (TNBC) cells. Co-treatment induces G0/G1 cell-cycle arrest, differentiation, and apoptosis, with VK2 increasing vitamin D receptor (VDR) expression in some cell lines, thereby boosting sensitivity23.
Cisplatin and Etoposide:
VK2 potentiates the effects of these chemotherapeutic agents by enhancing apoptosis and overcoming drug resistance. Preclinical studies suggest improved cell death rates when VK2 is combined with cisplatin or etoposide13.
All-trans Retinoic Acid (ATRA):
Case reports highlight complete remission in acute promyelocytic leukaemia patients treated with VK2 and ATRA. VK2 monotherapy also improved haematopoiesis in MDS and post-MDS AML patients19.
Vitamin D3:
A clinical pilot study showed improved therapeutic response rates in leukaemia patients when VK2 was combined with vitamin D39.
Preclinical evidence indicates VK2 enhances the efficacy of traditional chemotherapeutics in these cancers by promoting apoptosis and mitigating drug resistance1012.
Overcoming Drug Resistance:
VK2 inhibits P-glycoprotein, a key mediator of multidrug resistance, and suppresses NF-κB pathways linked to chemoresistance68.
Metabolic Modulation:
VK2 induces metabolic stress in cancer cells, sensitising them to chemotherapy16.
Safety Advantage:
Unlike vitamin K3, VK2 exhibits no toxicity at high doses, making it ideal for combination regimens10.
A randomised controlled trial in HCC patients found VK2 (45–90 mg/day) safe and effective when combined with sorafenib or other agents514.
Case reports and pilot studies support VK2’s role in improving prognosis and reducing recurrence in liver cancer and leukaemia19.
| Cancer Type | Combined Agent(s) | Mechanism of Action | Outcome |
|---|---|---|---|
| Hepatocellular | Sorafenib, 5-FU | Cell-cycle arrest, NF-κB suppression | Synergistic tumour suppression156 |
| Breast (TNBC) | 1,25(OH)₂D₃ | VDR upregulation, differentiation | Enhanced apoptosis23 |
| Ovarian | Cisplatin, etoposide | Apoptosis induction, resistance reversal | Improved cell death13 |
| Leukaemia/MDS | ATRA, vitamin D3 | Haematopoiesis support, differentiation | Remission, reduced blastic cells19 |
| Pancreatic/Lung | Conventional chemo | P-glycoprotein inhibition | Reduced drug resistance810 |
In conclusion, VK2’s ability to enhance conventional therapies while minimising toxicity positions it as a promising adjunct in cancer treatment.
Further large-scale clinical trials are needed to validate these findings and establish optimal dosing protocols.
Vitamin K2 (VK2), even at therapeutic (high) doses used in cancer settings, appears to have a favourable impact on quality of life, with minimal side effects and several potential benefits supported by both clinical reports and animal studies.
Improved Haematological Function and Independence
In case reports, VK2 treatment in patients with myelodysplastic syndrome (MDS) led to significant improvements, such as alleviation of pancytopenia and elimination of the need for red-cell transfusions after 14 months of daily use. This indicates a direct positive effect on daily functioning and independence for patients with blood cancers1.
Remission and Disease Control
VK2, especially in combination with other agents (like all-trans retinoic acid), has been associated with complete remission in some leukaemia cases and suppression of tumour recurrence in liver cancer. This can translate to reduced disease burden, fewer symptoms, and potentially longer periods of stable health13.
Minimal Side Effects and Good Tolerability
Across multiple studies and case reports, VK2 has not been associated with significant adverse effects, even at high doses used in cancer therapy. Animal studies reinforce this, showing no observable negative impact on weight, appearance, or behaviour, suggesting that VK2 does not impair quality of life through toxicity or discomfort135.
Potential for Reduced Side Effects from Other Therapies
VK2 may enhance the efficacy of standard chemotherapeutics and, when used in combination, could allow for lower doses of more toxic drugs, potentially reducing the side effect burden and improving overall well-being1.
Cellular Protection and Reduced Oxidative Stress
VK2 has demonstrated antioxidant and anti-apoptotic properties in pre-clinical studies, protecting cells from oxidative damage and supporting cellular health. This could contribute to better energy levels and reduced fatigue, though direct clinical evidence in cancer patients is limited4.
No Impact on Coagulation at Therapeutic Doses
Even at high doses, VK2 does not induce a hypercoagulable state or significant changes in laboratory safety measurements, supporting its safety for long-term use5.
| Aspect | Observed Impact | Evidence Source |
|---|---|---|
| Haematological function | Improved, reduced transfusion need | Clinical case reports1 |
| Disease control/remission | Achievable in some cases | Clinical case reports13 |
| Side effects | Minimal to none | Clinical/animal studies135 |
| Daily functioning | Maintained or improved | Clinical/animal studies13 |
| Combination therapy benefits | Potentially fewer side effects overall | Clinical reports1 |
| Coagulation risk | No increase at high doses | Clinical studies5 |
For patients taking VK2 at therapeutic levels for cancer, current evidence suggests a neutral to positive impact on quality of life. VK2 is well tolerated, does not introduce significant side effects, and may improve disease-related symptoms and independence, especially in haematological cancers. While more systematic quality of life data from large trials would be valuable, the available evidence supports VK2 as a safe adjunct or alternative therapy with the potential for meaningful quality of life benefits135.
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Vitamin K2 is widely available as a dietary supplement. However, it has not been established as a treatment for cancer and more studies are required to validate the current findings.
No specific patient demographic has been definitively established as most likely to benefit from vitamin K2 (VK2) therapy for cancer, but several trends and risk groups have emerged from clinical, epidemiological, and preclinical studies:
1. Patients with Liver Disease or Cirrhosis
Multiple studies and case reports highlight VK2’s potential to reduce the risk of hepatocellular carcinoma (HCC) and suppress tumour recurrence in patients with chronic liver disease, cirrhosis (including type C cirrhosis), and those who have undergone curative hepatectomy for HCC5. VK2 supplementation may be especially beneficial for these high-risk groups.
2. Patients with Myelodysplastic Syndromes and Certain Leukaemias
Case reports and small clinical studies indicate that VK2 can improve haematopoiesis and reduce the need for transfusions in elderly patients with myelodysplastic syndrome (MDS) and post-MDS acute myeloid leukaemia (AML)5. VK2 has also been used in combination with other agents in relapsed acute promyelocytic leukaemia, suggesting a role in select haematological malignancies.
3. Populations with Sub-Optimal Vitamin K Status
Sub-optimal vitamin K status is common, particularly in older adults, and may be linked to higher risk of chronic diseases, including cancer1. Therefore, older individuals or those with poor dietary vitamin K intake could potentially benefit more from supplementation.
4. Patients at High Risk of Prostate and Lung Cancer
Epidemiological data suggest that higher dietary intake of VK2 is associated with a reduced risk of developing prostate and lung cancers5. These findings point to possible preventive benefits in populations at elevated risk for these cancers.
5. General Population and Cancer Mortality
Observational studies have found that individuals with the highest intakes of VK2 were significantly less likely to die from a range of cancers compared to those with the lowest intakes6. This suggests a possible broad preventive effect, though causality is not established.
6. Breast Cancer: A Note of Caution
Not all evidence is favourable. A large US study found that higher total menaquinone (vitamin K2) intake was associated with an increased risk of breast cancer incidence and mortality23. This suggests that VK2 supplementation may not be universally beneficial and that individual cancer types and patient characteristics must be considered.
| Demographic/Condition | Evidence for VK2 Benefit | Notes/Exceptions |
|---|---|---|
| Chronic liver disease/cirrhosis | Reduced HCC risk and recurrence | Strongest clinical evidence5 |
| Myelodysplastic syndromes/leukaemia | Improved haematopoiesis, remission cases | Case reports, small trials5 |
| Older adults/sub-optimal K status | Potential reduced cancer risk | Observational data1 |
| High risk of prostate/lung cancer | Lower incidence with higher VK2 intake | Epidemiological data5 |
| General population | Lower overall cancer mortality | Observational, not causal6 |
| Breast cancer | Possible increased risk with high VK2 | Large cohort study23 |
While VK2 shows promise for cancer prevention and therapy in certain high-risk groups—especially those with liver disease, MDS, or poor vitamin K status—no universal demographic has been established. Furthermore, potential risks in specific cancers (notably breast cancer) highlight the need for personalised assessment and further research before broad recommendations can be made.
Several resistance markers affecting vitamin K2 (VK2) efficacy in cancer treatment have been identified, primarily linked to genetic, metabolic, or cellular pathway alterations.
Key findings include:
SK-OV-3 Cell Line Resistance
The SK-OV-3 ovarian cancer cell line demonstrates intrinsic resistance to VK2, unlike the sensitive PA-1 cell line. While the exact mechanism remains unclear, differences in apoptotic pathway activation or metabolic processing of VK2 may contribute3.
HSD17β4 Overexpression
Overexpression of 17β-hydroxysteroid dehydrogenase 4 (HSD17β4) promotes HCC proliferation. VK2 binds directly to HSD17β4, inhibiting MEK/ERK and Akt pathways. Tumours with elevated HSD17β4 may require higher VK2 doses for efficacy4.
GGCX and VKORC1 Upregulation
In imatinib-resistant CML, gamma-glutamyl carboxylase (GGCX) and vitamin K epoxide reductase complex subunit 1 (VKORC1) are upregulated. These genes are critical for vitamin K recycling, and their overexpression may reduce VK2 bioavailability, diminishing its therapeutic effects5.
Bcl-2 Overexpression
High Bcl-2 levels in leukemic cells shift VK2’s action from apoptosis to autophagy, reducing cell death. This suggests Bcl-2 expression as a resistance marker in haematological malignancies4.
While not directly relevant to cancer, studies in methicillin-resistant Staphylococcus aureus (MRSA) show that sub-MIC VK2 incompletely inhibits fluoroquinolone resistance genes (norA, grlA, grlB, gyrA, gyrB), highlighting potential cross-resistance mechanisms in other contexts2.
| Cancer Type | Marker/Mechanism | Impact on VK2 Efficacy | Source |
|---|---|---|---|
| Ovarian | SK-OV-3 intrinsic resistance | No growth inhibition observed | 3 |
| HCC | HSD17β4 overexpression | Requires higher VK2 doses | 4 |
| CML | GGCX, VKORC1 upregulation | Reduces VK2 bioavailability | 5 |
| Leukaemia | Bcl-2 overexpression | Shifts response to autophagy | 4 |
Resistance to VK2 in cancer is influenced by genetic and metabolic markers such as GGCX, VKORC1, HSD17β4, and Bcl-2, as well as cell line-specific factors (e.g., SK-OV-3). These markers highlight the need for personalised dosing and combination therapies to overcome resistance. Further research is required to validate these findings and identify additional biomarkers.
Pre-clinical studies have extensively investigated VK2’s anti-cancer properties across multiple cancer types, including hepatocellular carcinoma (HCC), bladder cancer, colorectal cancer (CRC), leukaemia, and ovarian cancer.
Below is a summary of key findings from in vitro and in vivo studies:
Hepatocellular Carcinoma (HCC)
Bladder Cancer
VK2 promoted glycolysis via the PI3K/AKT/HIF-1α pathway, leading to metabolic stress and AMPK-dependent autophagic cell death under glucose-limited conditions4.
Colorectal Cancer (CRC)
VK2, alongside vitamins K3 and K5, induced apoptosis in CRC cells. While K3 and K5 showed stronger effects, VK2 was safer and non-toxic5.
Leukaemia
VK2 synergised with all-trans retinoic acid (ATRA) to induce differentiation and apoptosis in leukaemia cells2.
HCC Xenografts
Bladder Cancer Xenografts
VK2 (10–20 mg/kg) reduced tumour volume and extended survival in mice, linked to autophagic cell death and AMPK activation4.
CRC Xenografts
Intravenous VK2 (2 mM) inhibited tumour growth in mice, with apoptosis observed in treated tumours5.
| Mechanism | Cancer Type | Outcome |
|---|---|---|
| Cell-cycle arrest | HCC, CRC | G1 phase arrest via cyclin D1/CDK4 downregulation23 |
| Apoptosis induction | CRC, leukaemia | Caspase-3 activation and DNA fragmentation25 |
| Autophagic cell death | Bladder cancer | AMPK/mTORC1 pathway modulation under metabolic stress4 |
| Metabolic reprogramming | Bladder cancer | Glycolysis promotion and TCA cycle suppression4 |
| Pathway inhibition | HCC | MEK/ERK and Akt suppression via HSD17β4 binding3 |
No toxicity observed in animal models, even at high doses (e.g., 45 mg/kg in HCC studies)23.
Unlike vitamin K3 (menadione), VK2 showed no adverse effects, making it a safer candidate for clinical translation5.
Pre-clinical trials demonstrate VK2’s broad anti-cancer efficacy through diverse mechanisms, including cell-cycle arrest, apoptosis, autophagy, and metabolic modulation. Its excellent safety profile in animal models supports further clinical exploration, particularly in HCC, bladder cancer, and CRC. However, most studies remain in early stages, with a need for phase III trials to validate these findings.
Vitamin K2 has been evaluated in several clinical trials, including cancer-related studies and other health conditions, but as of April 2025, it is not part of any large, ongoing late-phase (phase III or IV) cancer clinical trials.
Here is a summary of the relevant clinical trial evidence:
Phase II Cancer Trials:
Vitamin K2 has been tested in phase II clinical trials for myelodysplastic syndromes (MDS), a pre-leukaemic blood disorder. In these studies, VK2 (45 mg/day) was used as monotherapy and in combination with vitamin D3 (alfacalcidol). The trials found that VK2, especially when combined with vitamin D3, improved anaemia and thrombocytopenia in patients with low or intermediate-1 risk MDS. These were open-label, single-arm, and multicentre phase II trials35. There is no evidence from these or other sources of phase III or IV trials for cancer indications.
Other Conditions:
Recent and ongoing clinical trials of vitamin K2 have focused on non-cancer indications, such as nocturnal leg cramps (randomised controlled trial, not oncology-related)2, COVID-19 (phase II, double-blind, randomised, placebo-controlled trial)4, and bone health1. The COVID-19 trial is phase II, but recruitment has stopped and the primary focus is not cancer.
Combination Therapy:
The phase II MDS trials included both VK2 monotherapy and VK2 plus vitamin D3 combination therapy, with the combination showing a higher response rate35.
Summary Table: Vitamin K2 Clinical Trials (Cancer Focus)
| Indication | Phase | Status | Combination | Outcome/Notes |
|---|---|---|---|---|
| Myelodysplastic Synd. | II | Completed | With/without Vit D3 | Improved anaemia/thrombocytopenia; safe35 |
| Other cancers | — | No current trials | — | No phase III/IV cancer trials identified |
Conclusion
Vitamin K2 has been tested in phase II clinical trials for blood cancers (specifically MDS), both as monotherapy and in combination with vitamin D3, with promising results and good safety. However, there are currently no active or recently completed phase III or IV cancer clinical trials involving vitamin K2. Most ongoing vitamin K2 trials focus on non-cancer conditions.
Several genetic markers have been identified that influence vitamin K2 (VK2) metabolism, bioavailability, and efficacy. These polymorphisms affect enzymes and proteins involved in vitamin K cycling, drug interactions, and biological responses.
Key findings include:
rs2108622 (1297G>A)
This polymorphism significantly affects plasma vitamin K1 (VK1) and menaquinone-4 (MK-4) levels. Individuals with the AA genotype have higher plasma concentrations of VK1 and MK-4 compared to those with GG or GA genotypes. This suggests that CYP4F2 genetic variants may influence dietary or supplemental VK2 requirements for optimal efficacy5.
Variants in VKORC1 (e.g., rs9923231) are strongly associated with warfarin sensitivity and vitamin K metabolism. These polymorphisms alter the enzyme’s ability to recycle vitamin K, affecting both anticoagulant therapy and VK2’s ability to counteract warfarin’s effects5.
Polymorphisms like CYP2C9 rs1057910 influence warfarin metabolism and vitamin K status. Poor metabolisers (e.g., CYP2C9 *2/*3 alleles) require lower warfarin doses and may experience heightened VK2 deficiency risks, impacting bone and cardiovascular health5.
Genetic variations in SXR/PXR, a nuclear receptor activated by VK2, may modulate its transcriptional regulation of bone-specific genes (e.g., osteocalcin). This affects VK2’s efficacy in promoting bone mineralisation and combating osteoporosis4.
While not directly studied in the provided sources, APOE polymorphisms (e.g., ε4 allele) are linked to altered lipid metabolism and vitamin K transport, potentially influencing VK2’s absorption and tissue distribution.
Personalised Supplementation: Individuals with CYP4F2 AA genotypes may require lower VK2 doses to achieve therapeutic effects, while those with GG/GA genotypes might need higher intake.
Anticoagulant Interactions: VKORC1 and CYP2C9 variants necessitate careful VK2 dosing in patients on warfarin to avoid thrombosis or bleeding risks56.
Bone Health: SXR/PXR polymorphisms could explain variability in VK2’s effectiveness in improving bone mineral density48.
| Gene | Polymorphism | Impact on VK2 Efficacy | Clinical Relevance |
|---|---|---|---|
| CYP4F2 | rs2108622 (G>A) | AA genotype ↑ plasma VK1/MK-4 levels | Dose adjustment for supplementation |
| VKORC1 | rs9923231 | Alters vitamin K recycling; affects warfarin interaction | Critical for anticoagulant management |
| CYP2C9 | rs1057910 | Alters warfarin metabolism, impacting VK2 status | Risk of VK2 deficiency in poor metabolisers |
| SXR/PXR | Variants unspecified | Modulates VK2’s transcriptional activity in bone | Bone health outcomes variability |
Genetic markers in CYP4F2, VKORC1, CYP2C9, and SXR/PXR significantly influence VK2’s efficacy, particularly in contexts of anticoagulation therapy and bone health. These findings underscore the potential for genetic testing to guide personalised VK2 supplementation and improve therapeutic outcomes.
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Drugs and supplements with anti-inflammatory properties help reduce inflammation, thereby lowering the risk of cancer and other chronic diseases.
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