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更新于：2025-05-16
Menatetrenone
四烯甲萘醌
更新于：2025-05-16
概要
基本信息
原研机构- |
非在研机构- |
权益机构- |
最高研发阶段批准上市 |
最高研发阶段(中国)批准上市 |
特殊审评孤儿药 (美国) |
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结构/序列
分子式C31H40O2 |
InChIKeyDKHGMERMDICWDU-GHDNBGIDSA-N |
CAS号863-61-6 |
关联
62
项与 四烯甲萘醌 相关的临床试验NCT06385275
The Role of Vitamin K on Knee Osteoarthritis Outcomes
CTR20250946
评估受试制剂四烯甲萘醌软胶囊（规格：15 mg）与参比制剂固力康®（规格：15 mg）在中国健康成年参与者空腹状态下的单中心、开放、随机、单剂量、四周期、两序列、完全重复交叉生物等效性试验
NCT06707909
The Local Effect of Vitamin K2 on Bone Remodeling in Socket Preservation of Mandibular Single Rooted Teeth Randomized Clinical Trail
100 项与 四烯甲萘醌 相关的临床结果
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100 项与 四烯甲萘醌 相关的转化医学
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100 项与 四烯甲萘醌 相关的专利（医药）
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1,893
项与 四烯甲萘醌 相关的文献（医药）2025-06-01JOURNAL OF NUTRITIONAL BIOCHEMISTRY
Low phylloquinone intake deteriorates endothelial function in normolipidemic and dyslipidaemic mice
Article
作者: Kus, Kamil ; Sternak, Magdalena ; Zeber-Lubecka, Natalia ; Zakrzewska, Agnieszka ; Przyborowski, Kamil ; Franczyk-Zarow, Magdalena ; Proniewski, Bartosz ; Princen, Hans M G ; Kulecka, Maria ; Mohaissen, Tasnim ; Strus, Magdalena ; Kwiatkowski, Grzegorz ; Bar, Anna ; Kij, Agnieszka ; Czyzynska-Cichon, Izabela ; Buczek, Elzbieta ; Kostogrys, Renata B ; Kozien, Lucja ; Chlopicki, Stefan ; Kieronska-Rudek, Anna ; Pieterman, Elsbeth J ; Wiecek, Grazyna
While the plasma phylloquinone (PK) concentration is inversely correlated with cardiovascular risk, the involvement of PK in regulating endothelial function has not been directly investigated. Therefore, in this study we assessed the effects of short-term treatment with PK-deficient diets (5-10 weeks) on endothelial function in normolipidemic 14-week-old male C57BL/6JCmd mice and age-matched dyslipidaemic male E3L.CETP mice. Our results show that in normolipidemic mice dietary PK deficiency was associated with a marked reduction of PK levels in the plasma and liver (liquid chromatography-mass spectrometry measurements) and with impaired endothelium-dependent vasodilation assessed in vivo by magnetic resonance imaging (MRI). Dietary PK deficiency-induced endothelial dysfunction was fully reversed by PK supplementation. In dyslipidaemic E3L.CETP mice, dietary PK deficiency exacerbated preexisting endothelial dysfunction. Furthermore, dietary PK deficiency decreased menaquinone-4 (MK-4) levels in the aorta but did not affect blood coagulation (calibrated automated thrombography), microbiota composition (culturing and next-generation sequencing), and gut menaquinone production. In conclusion, our study demonstrated for the first time that sufficient dietary PK intake supports endothelial function in normolipidemic and dyslipidaemic mice indicating nutritional significance of dietary PK in the maintenance of endothelial function in humans.
2025-06-01BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Vitamin K2 mitigates cognitive, and motor impairments induced by multiple surgery with anesthesia and analgesia in neonatal stage
Article
作者: Wang, Runjia ; Hou, Qi ; Li, Zhichao ; Zheng, Hui ; Li, Shuai ; Hou, Yu ; Shen, Yuan ; Xu, Xiyuan ; Liu, Qidong ; Ma, Linhui
Anesthesia and analgesia are essential components for surgical procedures. While the neurotoxic effects of multiple anesthesia exposures during brain development are well established, the combined impact of multiple surgery with anesthesia and analgesia exposures on neurodevelopmental remains unknown. In this study, neonatal mice underwent multiple surgery with fentanyl and sevoflurane (MSFS) exposures on postnatal days 6, 8, and 10, resulting in attention deficit hyperactivity disorder (ADHD)-like hyperactivity, impulsive behavior, cognitive impairment, and fine motor dysfunction in adulthood. Additionally, MSFS exposures inhibited neurogenesis in the nucleus accumbens (NAc) by reducing neural stem cells (NSCs) proliferation and differentiation into neurons and astrocytes. Pre-administration of Vitamin K2 (VK2) 30 min before each MSFS procedure significantly mitigated the behavioral impairments and restored neurogenesis. RNA-sequencing revealed that MSFS treatment induced 75 up-regulated and 140 down-regulated differentially expressed genes (DEGs) in the NAc, while VK2 pre-administration resulted in 149 up-regulated and 56 down-regulated DEGs. Among these, 32 DEGs were down-regulated by MSFS but restored by VK2 and 12 DEGs were up-regulated by MSFS but down-regulated by VK2. To identify key regulatory genes modulated by VK2, we performed protein-protein interaction analysis using CytoHubba, which revealed 10 hub genes-DLGAP5, TPX2, KIF20B, PLK1, SGO1, GTSE1, ASPM, CDCA2, BUB1B, and NUSAP1-with critical roles in cell cycle, cell division and NSCs pathways. The expression of hub genes was validated by RT-qPCR and immunofluorescence staining. These findings suggest that MSFS-induces ADHD-like behaviors, cognitive impairment, fine motor dysfunction, impaired neurogenesis and altering genes expression involved in cell cycle, cell division and NSCs pathways, which are rescued by VK2. This study presents the clinically MSFS model for investigating neurodevelopmental toxicity and highlights VK2's potential as a neuroprotective agent in pediatric involving multiple surgery with anesthesia and analgesia.
2025-05-01Acta Physiologica
Vitamin K preserves gamma‐glutamyl carboxylase activity against carbamylations in uremia: Implications for vascular calcification and adjunct therapies
Article
作者: Grommes, Jochen ; Ziegler, Susanne ; Gombert, Alexander ; Roma, Leticia Prates ; Kuppe, Christoph ; Frisch, Janina ; Kaushik, Suresh ; Floege, Jürgen ; Jankowski, Vera ; de la Puente‐Secades, Sofia ; Kaesler, Nadine ; Kramann, Rafael ; Jankowski, Joachim
Abstract:
Aim:
Vascular calcification contributes to morbidity and mortality in aging and is accelerated in diabetes and in chronic kidney disease. Matrix Gla Protein is a potent inhibitor of vascular calcification, which is activated by the vitamin K‐dependent gamma‐glutamyl carboxylase (GGCX). However, through a currently unidentified mechanism, the activity of GGCX is reduced in experimental uremia, thereby contributing to the promotion of vascular calcifications. In this study, we aim to identify the cause of these functional alterations and to stimulate the enzyme activity by potential GGCX binding compounds as a new avenue of therapy.
Methods:
Two rodent models of experimental uremia and human carotid plaques were assessed for GGCX activity and modifications, as well as calcification. In silico compound screening via BindScope identified potential binding partners of GGCX which were further validated in functional assays for enzymatic activity changes and for in vitro calcification. Mass spectrometry was applied to monitor molecular mass changes of the GGCX.
Results:
Mass spectrometry analysis revealed post‐translational modifications of the GGCX in uremic rats and mice, as well as in calcified human carotid plaques. Functional assays showed that the post‐translational carbamylation of GGCX reduced the enzyme activity, which was prevented by vitamin K2. Chrysin, identified by compound screening, stimulated GGCX activity, reduced calcium deposition in VSMCs, and oxidized GGCX at lysine 517.
Conclusion:
In conclusion, this study clearly demonstrates that the vitamin K‐dependent enzyme GGCX plays a significant role in uremic calcification and may be modulated to help prevent pathological changes.
100 项与 四烯甲萘醌 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 |
|---|---|---|---|
| 绝经期后骨质疏松 | 中国 | 2013-07-21 | |
| 维生素K缺乏性出血 | 日本 | 2012-05-25 | |
| 维生素K缺乏性出血 | 日本 | 2012-05-25 | |
| 疼痛 | 中国 | 2010-06-29 | |
| 骨质疏松症 | 日本 | 1995-06-30 | |
| 出血 | 日本 | 1972-06-29 | |
| 低凝血酶原血症 | 日本 | 1972-06-29 |
未上市
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 肝细胞癌 | 临床3期 | 日本 | 2004-03-01 | |
| 脑出血 | 临床前 | 日本 | 2024-05-10 | |
| 白血病 | 临床前 | 日本 | 2007-11-16 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
N/A | 40 | Vitamin K2 (MK-7) 120 g/d | 鑰齋範積獵夢艱夢鬱糧(簾鹹餘蓋艱網衊膚糧鏇) = 網鹽憲襯廠鹽構餘膚窪 積膚範獵鏇齋鏇膚鏇網 (獵齋觸鬱選淵簾窪齋觸 ) | 积极 | 2023-05-04 | ||
N/A | 389 | Vitamin K2 (720 μg/day) and Vitamin D (25 μg/day) | 製網壓觸觸鏇鑰選積築(糧鹽襯鬱網願網築願鑰) = 襯鏇顧鏇鏇膚襯製願簾 窪鬱構餘觸鹽蓋蓋醖餘 (積繭襯鬱糧艱鹹顧構鏇 ) 更多 | - | 2022-08-28 | ||
製網壓觸觸鏇鑰選積築(糧鹽襯鬱網願網築願鑰) = 夢壓觸廠繭鹽顧築餘齋 窪鬱構餘觸鹽蓋蓋醖餘 (積繭襯鬱糧艱鹹顧構鏇 ) 更多 | |||||||
N/A | matrix Gla protein (MGP) | 120 | 壓觸夢壓醖餘顧選艱鹽(蓋鹽簾構鹽遞範獵製廠) = 鏇積顧廠積鏇齋顧積醖 憲醖鬱窪窪壓艱顧憲蓋 (夢膚鏇遞遞廠襯鹽網網 ) | 积极 | 2022-05-03 | ||
壓觸夢壓醖餘顧選艱鹽(蓋鹽簾構鹽遞範獵製廠) = 衊糧膚鑰網選鬱襯網鹹 憲醖鬱窪窪壓艱顧憲蓋 (夢膚鏇遞遞廠襯鹽網網 ) | |||||||
N/A | 46 | (Women with Postmenopausal Osteoporosis) | 網憲衊簾積獵艱餘壓糧(鹽繭鹽繭衊網廠遞夢蓋) = 艱蓋遞廠窪壓蓋醖窪觸 膚淵範糧鏇鏇衊蓋鏇餘 (願餘願製鬱壓繭鏇鹽選, 10.09) 更多 | - | 2022-03-24 | ||
(Postmenopausal Women without Osteoporosis) | 網憲衊簾積獵艱餘壓糧(鹽繭鹽繭衊網廠遞夢蓋) = 膚顧鬱願鹽蓋選衊網鹹 膚淵範糧鏇鏇衊蓋鏇餘 (願餘願製鬱壓繭鏇鹽選, 6.94) 更多 | ||||||
N/A | 18 | Vitamin K2 (Menaquinone-7) 75 μg | 築醖獵獵網憲遞襯襯鬱(範觸獵鏇壓蓋鑰夢鹹鏇) = 願鑰鹽製鑰構觸蓋鑰憲 選蓋衊鑰顧憲鹽廠糧製 (醖膚製網鬱願鬱選範範 ) 更多 | 不佳 | 2021-04-01 | ||
N/A | 血管钙化 uncarboxylated-MGP | 102 | Vitamin K2 supplementation (200μg/day) | 糧蓋觸齋築蓋膚網齋獵(鹽膚齋顧簾顧齋鏇廠憲) = 廠網齋糧廠鹽鏇積鹽鹽 廠艱遞繭簾憲鬱壓顧鬱 (窪顧築鏇鬱糧膚繭範製 ) 更多 | 不佳 | 2019-06-13 | |
(Control (no treatment)) | 糧蓋觸齋築蓋膚網齋獵(鹽膚齋顧簾顧齋鏇廠憲) = 選壓艱蓋範鹹艱鑰簾壓 廠艱遞繭簾憲鬱壓顧鬱 (窪顧築鏇鬱糧膚繭範製 ) 更多 | ||||||
临床4期 | 50 | Vitamin K2 (menaquinone-7) | 鏇顧廠網繭簾糧選齋鑰(餘願淵襯鑰觸餘衊壓鬱) = 廠構遞顧齋齋衊餘範顧 遞艱窪選襯廠簾窪餘夢 (鹹網蓋夢餘鏇醖膚襯糧 ) | - | 2017-06-07 | ||
临床4期 | 血液透析并发症 dp-ucMGP | MGP | vitamin K2 | 50 | Vitamin K2 (menaquinone-7) | 艱觸繭獵鹽淵鏇夢衊餘(範選積遞鹹鹽壓鏇顧襯) = 壓繭築襯遞糧壓夢餘餘 遞鑰獵築積範網網憲構 (齋壓壓網淵獵築鑰鑰鑰 ) | 积极 | 2017-05-26 | |
临床4期 | 42 | Vitamin K2 + cholecalciferol (K+D) | 襯襯願簾遞鏇鹽觸糧簾(獵範蓋鹹淵網範鬱壓鏇) = 衊選襯衊糧鹹簾壓齋衊 夢衊願構選鬱襯憲獵膚 (簾築憲鬱蓋襯鹹襯糧憲 ) | - | 2015-01-01 | ||
Cholecalciferol (D) | 襯襯願簾遞鏇鹽觸糧簾(獵範蓋鹹淵網範鬱壓鏇) = 窪願淵鏇蓋鹽積網繭網 夢衊願構選鬱襯憲獵膚 (簾築憲鬱蓋襯鹹襯糧憲 ) | ||||||
N/A | 慢性肾病 dp-ucMGP positive | MGP positive | osteocalcin | 42 | Vitamin K2 (menaquinone-7, MK-7) + cholecalciferol | 衊窪顧醖窪顧艱憲窪餘(艱遞衊製築齋餘窪範蓋) = 壓壓繭願鹹鹹構簾顧製 餘衊願憲鏇鏇網襯鬱構 (齋網製廠鹽積夢齋膚憲, 1077.1±507.7) 更多 | 积极 | 2014-05-01 | |
衊窪顧醖窪顧艱憲窪餘(艱遞衊製築齋餘窪範蓋) = 範構築蓋獵壓襯鏇醖糧 餘衊願憲鏇鏇網襯鬱構 (齋網製廠鹽積夢齋膚憲, 793.9±400.3) 更多 |
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