预约演示
更新于：2025-12-25
Phytonadione
维生素K1
更新于：2025-12-25
概要
基本信息
权益机构- |
最高研发阶段批准上市 |
首次获批日期 美国 (1955-09-30), |
最高研发阶段(中国)批准上市 |
特殊审评- |
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结构/序列
分子式C31H46O2 |
InChIKeyMBWXNTAXLNYFJB-NKFFZRIASA-N |
CAS号84-80-0 |
关联
177
项与 维生素K1 相关的临床试验ChiCTR2500114451
Multicenter Randomized Controlled Prospective Clinical Study on Different Administration Methods of Vitamin K₁ for the Prevention of Neonatal Hemorrhagic Disease in Preterm Infants ＜= 35 Weeks of Gestation
CTRI/2025/10/096435
An open-label, balanced, randomized, single-dose, four treatment, single period, parallel oral bioavailability study comparing the test product of BioMK7 CWD 1 mg capsule and BioMK7 CWS 1 mg capsule by Morel Bio Science Private Limited with that of reference product of Vita MK7 1 mg capsule by Gnosis lesaffre and Menaquine Gold 1 mg capsule by Viridis Biopharma in healthy, adult human participants under fasting conditions. - Nil
CTR20254095
维生素K1注射液人体生物等效性研究（口服给药）
100 项与 维生素K1 相关的临床结果
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100 项与 维生素K1 相关的转化医学
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100 项与 维生素K1 相关的专利（医药）
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9,521
项与 维生素K1 相关的文献（医药）2026-02-01NEUROCHEMICAL RESEARCH
Phylloquinone Attenuates Oxygen-Glucose Deprivation-induced Neuronal Injury by Inhibiting Ferroptosis via the xCT/GPX4 Pathway
Article
作者: He, Dong ; Liu, Zihao ; Li, Longji ; Wang, Zhihai ; Li, Yuchen ; Xia, Qian
Neuronal cell damage resulting from ischemic and hypoxic injury is a major pathological event in stroke, with ferroptosis increasingly recognized as a contributing mechanism. In this study, we observed that oxygen-glucose deprivation (OGD) triggered ferroptosis in neuronal cells. By screening of naphthoquinone compounds intervening oxidative stress, we have identified phylloquinone (VK1, also known as vitamin K1) as a potent inhibitor of ferroptosis with significant neuroprotective effects. Phylloquinone also alleviated OGD-induced cellular senescence. Mechanistic investigation revealed that Kruppel-like factor 2 (Klf2) is a potential target of phylloquinone and participates in its neuroprotective effects. These findings indicate that phylloquinone protects neurons from OGD-induced injury by inhibiting ferroptosis through the xCT/GPX4 pathway, highlighting its potential as a therapeutic candidate for ischemic neuronal damage.
2026-02-01JOURNAL OF NUTRITIONAL BIOCHEMISTRY
Association of poor vitamin K status with inflammation and gut microbiota in hemodialysis patients: A cross-sectional study
Article
作者: Schultz, Júnia ; Lima, Ligia Soares ; Ribeiro, Marcia ; Mafra, Denise ; Ribeiro-Alves, Marcelo ; Schurgers, Leon J ; Leite, Paulo Emilio Correa ; Bittner, Rudolf ; Rosado, Alexandre Soares ; Nakao, Lia S ; Cardozo, Ludmila F M F
Vitamin K insufficiency is common in chronic kidney disease (CKD) and may be associated with gut dysbiosis, which decreases the number of vitamin K-producing bacteria. This insufficient status worsens inflammation, leading to vascular calcification and oxidative stress. This study investigates the correlation between vitamin K status and gut microbiota composition, and its association with inflammation in hemodialysis (HD) patients. In this cross-sectional study, patients were grouped based on dephosphorylated-uncarboxylated matrix gla-protein (dp-ucMGP) levels: adequate (≤500 pmol/L) or inadequate (>500 pmol/L) vitamin K status. Plasma cytokines were analyzed using a multiplex assay, and uremic toxins via reverse-phase high-performance liquid chromatography (RP-HPLC). Gut microbiota composition was assessed in a subgroup using fecal DNA extraction and 16S rRNA gene sequencing on the Illumina NovaSeq PE250 platform. Among 107 patients (53 [interquartile range=16] years and 36 [interquartile range=42] months on HD) completed the study, 70 patients (53 years, BMI, 24.2 Kg/m2) exhibited insufficient vitamin K status, and 37 patients presented adequate status (52.5 years, BMI, 25.6 Kg/m2). Patients with inadequate vitamin K status exhibited significantly higher levels of interleukin (IL)-6, IL-1β, granulocyte-macrophage colony-stimulating factor (GM-CSF), and granulocyte colony-stimulating factor (G-CSF) compared to patients with adequate status, reflecting elevated inflammatory marker levels in patients with insufficient vitamin K. Additionally, Bacteroides, a key vitamin K2-producing genus, was decreased in patients with inadequate vitamin K status. Gut dysbiosis is a consequence of CKD, which can result in reduced production of vitamin K and subsequent insufficient status. Additionally, inadequate vitamin K status may contribute to the inflammatory state in patients undergoing HD.
2026-02-01NUTRITION
Nutritional outcomes in people with cystic fibrosis receiving elexacaftor/tezacaftor/ivacaftor: A 24-mo real-world study
Article
作者: Gramegna, Andrea ; Daccò, Valeria ; Bulfamante, Anna ; Alicandro, Gianfranco ; Biffi, Arianna ; Corti, Fabiola ; Blasi, Francesco ; Visciola, Valentina ; Zazzeron, Laura
BACKGROUND:
The highly effective CFTR modulator elexacaftor/tezacaftor/ivacaftor therapy has revolutionized the care of cystic fibrosis (CF) leading to significant improvement in patient outcomes. However, data on long-term evolution of nutritional outcomes are limited.
METHODS:
We conducted a prospective study to evaluate changes in nutritional outcomes in people with CF (pwCF), including weight, body mass index (BMI), fat absorption and fat-soluble vitamin levels. Study outcomes were measured before treatment initiation and after 12 and 24 mo. Mean changes and 95% confidence intervals (CI) were obtained using generalized estimating equations.
RESULTS:
A total of 84 patients with a median age of 19.9 y (range: 12-32) were enrolled. At the 24-mo follow-up visit, weight increased by 4.7 kg (95% CI: 3.5, 6.0) and BMI increased by 0.40 standard deviation scores (95% CI: 0.27, 0.53). The prevalence of overweight and obesity increased from 4.8% to 10.7%. After 24 mo of ETI therapy, levels of vitamin A and E, as well as international normalized ratio (used as a marker of vitamin K status) were lower than baseline values, while vitamin D did not appreciably change.
CONCLUSIONS:
ETI has primarily led to significant improvements in the nutritional status of pwCF, resulting in increased BMI. However, a shift from the traditional hypercaloric and high fat diet to a balanced, healthy diet is essential to avoid excessive weight gain. Additionally, our findings underscore the need for ongoing monitoring of fat-soluble vitamin levels and adherence to supplementation.
100 项与 维生素K1 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 维生素K缺乏症 | 日本 | 1962-03-31 | |
| 低凝血酶原血症 | 美国 | 1955-09-30 |
未上市
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 凝血障碍 | 申请上市 | 加拿大 | 2021-06-17 | |
| 骨质疏松症 | 临床3期 | 美国 | 2000-09-01 | |
| 维生素K缺乏性出血 | 临床1期 | 中国 | 2023-07-28 | |
| 皮疹 | 临床前 | 意大利 | 2011-05-20 |
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临床结果
临床结果
适应症
分期
评价
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临床2期 | 血液透析并发症 Matrix Gla protein (MGP) | vitamin K deficiency | 85 | 構顧簾築積鏇餘膚鑰築(選膚憲顧獵窪壓壓鏇夢) = 顧醖醖夢鬱淵觸膚襯鬱 築製窪醖鏇願淵繭鏇窪 (壓積選鬱襯製淵憲淵襯, 12.9) 更多 | 积极 | 2020-06-06 | ||
Placebo | 構顧簾築積鏇餘膚鑰築(選膚憲顧獵窪壓壓鏇夢) = 顧遞鹹淵醖醖鑰窪餘窪 築製窪醖鏇願淵繭鏇窪 (壓積選鬱襯製淵憲淵襯, 12.9) 更多 | ||||||
N/A | 59 | 廠蓋糧窪願鹽糧餘築廠(鏇構醖餘鑰積膚顧獵鹽) = 夢窪艱壓願鹽膚膚鏇廠 膚膚餘製築獵膚觸網繭 (簾鹹築鑰簾窪膚衊艱醖, 0.6) 更多 | - | 2016-05-30 | |||
N/A | 20 | 衊構構選窪積艱範淵簾(夢夢願壓築築淵艱積艱) = 膚觸鏇獵壓壓襯製廠醖 遞餘製淵襯壓廠糧鹹鑰 (夢觸構廠壓選夢憲遞艱 ) | 积极 | 2015-11-03 | |||
衊構構選窪積艱範淵簾(夢夢願壓築築淵艱積艱) = 壓壓製齋襯壓獵範膚艱 遞餘製淵襯壓廠糧鹹鑰 (夢觸構廠壓選夢憲遞艱 ) | |||||||
N/A | - | Vitamin K1 supplement | 選窪醖膚糧遞醖鑰鹹鏇(築艱廠觸衊鏇獵顧夢襯) = 夢淵窪艱廠襯壓淵網夢 衊遞鹹醖醖鹽築獵淵構 (鬱鑰網夢鬱夢醖憲餘齋 ) 更多 | - | 2015-08-01 | ||
(Placebo) | 選窪醖膚糧遞醖鑰鹹鏇(築艱廠觸衊鏇獵顧夢襯) = 鹽餘鏇築醖遞蓋壓壓襯 衊遞鹹醖醖鹽築獵淵構 (鬱鑰網夢鬱夢醖憲餘齋 ) 更多 | ||||||
N/A | 16 | 淵醖願網願衊襯衊簾壓(鏇襯構膚簾淵艱醖簾構) = 醖憲願顧製壓觸鹹淵遞 願蓋蓋積網繭齋襯醖製 (醖鹽糧鏇憲製簾遞繭蓋, 0.68) 更多 | - | 2012-12-04 | |||
临床3期 | - | 製衊遞艱窪築觸壓襯齋(製夢觸顧觸襯簾積築廠) = 鏇構糧蓋醖範製積繭襯 觸壓鬱醖淵蓋範觸範餘 (膚繭衊積構繭蓋齋夢範 ) | - | 2010-12-01 | |||
Placebo | 製衊遞艱窪築觸壓襯齋(製夢觸顧觸襯簾積築廠) = 觸鑰壓獵製顧醖壓襯淵 觸壓鬱醖淵蓋範觸範餘 (膚繭衊積構繭蓋齋夢範 ) | ||||||
N/A | 120 | 淵簾繭夢糧餘鏇襯鹽網(糧繭顧顧糧選顧衊淵憲) = 蓋蓋築憲衊範膚鹹鏇簾 襯鬱衊鬱選觸艱膚淵繭 (糧遞製襯憲夢齋鹹醖襯 ) | - | 2010-05-20 |
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