Vitamin K
(Synonyms: 维生素K) 目录号 : GC32531
VitaminK是一组脂溶性维生素，对身体内许多蛋白质有重要功能，如凝血因子，骨钙素和基质-Gla蛋白。
Cas No.:12001-79-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Vitamin K is a group of fat soluble vitamins, important for the function of numerous proteins within the body, such as the coagulation factors, osteocalcin and matrix-Gla protein.
Phylloquinone (vitamin K1) and Menaquinones (vitamin K2) are the two naturally occurring forms of vitamin K. Phylloquionone is the major dietary source of vitamin K and is found at highest concentrations in green leafy vegetables[1]. Vitamin K2 (menaquinone) is found in small amounts in chicken, butter, egg yolks, cheese and fermented soyabeans. Vitamin K1 and vitamin K2 are required for the γ-glutamyl carboxylation of all vitamin K-dependent proteins[2]. Vitamin K has important actions in the nervous system. Vitamin K contributes to the biological activation of proteins Gas6 and protein S, ligands for the receptor tyrosine kinases of the TAM family (Tyro3, Axl, and Mer). In brain, vitamin K also participates in the synthesis of sphingolipids, an important class of lipids present in high concentrations in brain cell membranes[3].
Vitamin K is well-known for its function in blood coagulation. Several human studies report the beneficial role of vitamin K supplementation in improving insulin sensitivity and glucose tolerance, preventing insulin resistance, and reducing the risk of type 2 diabetes[1]. The adequate intake for vitamin K has been proposed to be 90 µg/day for women and 120 µg/day for men[2]. Vitamin K deficiency results in an increase in undercarboxylated osteocalcin, a protein with low biological activity. Several studies have demonstrated that low dietary vitamin K intake is associated with low bone mineral density or increased fractures. Additionally, vitamin K supplementation has been shown to reduce undercarboxylated osteocalcin and improve the bone turnover profile[4].
[1]. Manna P, et al. Beneficial role of vitamin K supplementation on insulin sensitivity, glucose metabolism, and the reduced risk of type 2 diabetes: A review. Nutrition. 2016 Jul-Aug;32(7-8):732-9. [2]. DiNicolantonio JJ, et al. The health benefits of vitamin K. Open Heart. 2015 Oct 6;2(1):e000300. [3]. Ferland G, et al. Vitamin K, an emerging nutrient in brain function. Biofactors. 2012 Mar-Apr;38(2):151-7. [4]. Bügel S, et al. Vitamin K and bone health. Proc Nutr Soc. 2003 Nov;62(4):839-43.
| Cas No. | 12001-79-5 | SDF | |
| 别名 | 维生素K | ||
| Canonical SMILES | [Vitamin K] | ||
| 分子式 | 分子量 | ||
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Vitamin K and osteoporosis: Myth or reality?
Metabolism 2017 May;70:57-71.PMID:28403946DOI:10.1016/j.metabol.2017.01.032.
Vitamin K is a liposoluble vitamin. The predominant dietary form, phylloquinone or vitamin K1, is found in plants and green vegetables; whereas menaquinone, or vitamin K2, is endogenously synthesized by intestinal bacteria and includes several subtypes that differ in side chain length. Aside from its established role in blood clotting, several studies now support a critical function of Vitamin K in improving bone health. Vitamin K is in fact required for osteocalcin carboxylation that in turn regulates bone mineral accretion; it seems to promote the transition of osteoblasts to osteocytes and also limits the process of osteoclastogenesis. Several observational and interventional studies have examined the relationship between Vitamin K and bone metabolism, but findings are conflicting and unclear. This systematic review aims to investigate the impact of Vitamin K (plasma levels, dietary intake, and oral supplementation) on bone health with a particular interest in bone remodeling, mineral density and fragility fractures.
Vitamin K - sources, physiological role, kinetics, deficiency, detection, therapeutic use, and toxicity
Nutr Rev 2022 Mar 10;80(4):677-698.PMID:34472618DOI:10.1093/nutrit/nuab061.
Vitamin K is traditionally connected with blood coagulation, since it is needed for the posttranslational modification of 7 proteins involved in this cascade. However, it is also involved in the maturation of another 11 or 12 proteins that play different roles, encompassing in particular the modulation of the calcification of connective tissues. Since this process is physiologically needed in bones, but is pathological in arteries, a great deal of research has been devoted to finding a possible link between Vitamin K and the prevention of osteoporosis and cardiovascular diseases. Unfortunately, the current knowledge does not allow us to make a decisive conclusion about such a link. One possible explanation for this is the diversity of the biological activity of Vitamin K, which is not a single compound but a general term covering natural plant and animal forms of Vitamin K (K1 and K2) as well as their synthetic congeners (K3 and K4). Vitamin K1 (phylloquinone) is found in several vegetables. Menaquinones (MK4-MK13, a series of compounds known as vitamin K2) are mostly of a bacterial origin and are introduced into the human diet mainly through fermented cheeses. Current knowledge about the kinetics of different forms of Vitamin K, their detection, and their toxicity are discussed in this review.
The mechanism of action of Vitamin K
Annu Rev Nutr 1995;15:419-40.PMID:8527228DOI:10.1146/annurev.nu.15.070195.002223.
Vitamin K is the blood-clotting vitamin. The mechanism of action of Vitamin K is discussed in terms of a new carbanion model that mimics the proton abstraction from the gamma position of protein-bound glutamate. This is the essential step leading to carboxylation and activation of the blood-clotting proteins. The model comprises an oxygenation that is coupled to carbon-carbon bond formation, as is the oxygenation of Vitamin K hydroquinone to Vitamin K oxide. The model hypothesis is also supported by the mechanism of inhibition of the carboxylase by HCN, which acts as an acid-base inhibitor rather than a metal-complexing inhibitor. The new model postulates a dioxetane intermediate that explains the presence of a second atom of 18O (from 18O2) incorporated into Vitamin K oxide in the course of the enzymatic carboxylation. Finally, the chemistry developed here has been used to define the active site of Vitamin K hydroquinone as the carbon-carbon bond adjacent to the methyl group.
Vitamin K deficiency
Southeast Asian J Trop Med Public Health 1993;24 Suppl 1:5-9.PMID:7886607doi
Vitamin K (phylloquinone, K1; menaquinone, K2) functions as an essential cofactor for the synthesis of the coagulation protein factors II, VII, IX, X and protein C and S by promoting a unique post-translational modification of specific glutamic acid residues to gamma-carboxylglutamic acid, thus mediating calcium binding to phospholipid surfaces. Vitamin K deficiency results in a depletion of liver stores of phylloquinone, decreased plasma levels of vitamin K1, increased levels of K1 epoxide, appearance of noncarboxylated protein (PIVKA), decreased levels of functioning vitamin K-dependent clotting factors and prolongation of the APTT, PT and thrombotest. When the progression of deficiency leads to abnormal clotting tests a generalized bleeding tendency occurs. Noncarboxylated prothrombin (PIVKA-II) determinations are a sensitive indicator of Vitamin K deficiency. Although Vitamin K deficiency can occur at any age (warfarin, fasting, antibiotic therapy, malabsorption syndromes) the major public health problem is related to prevention of early, classic and late hemorrhagic disease of the newborn (HDN). A single dose of oral or parenteral Vitamin K prevents classic HDN but the most effective way to prevent early HDN is by giving large doses to the mother prior to delivery (2 weeks). Late HDN in breastfed infant occurs with a prevalence of about 20 per 100,000 live births when no neonatal prophylaxis is given. Parenteral (1 mg) K1 prevents late HDN and single or repeated doses of oral Vitamin K reduces the incidence but does not eliminate all late HDN. The optimal (cost, feasibility, effective) mode of neonatal prophylaxis remains to be determined.
Vitamin K: A novel cancer chemosensitizer
Biotechnol Appl Biochem 2022 Dec;69(6):2641-2657.PMID:34993998DOI:10.1002/bab.2312.
Cancer incidences are growing rapidly and causing millions of deaths globally. Cancer treatment is one of the most exigent challenges. Drug resistance is a natural phenomenon and is considered one of the major obstacles in the successful treatment of cancer by chemotherapy. Combination therapy by the amalgamation of various anticancer drugs has suggested modulating tumor response by targeting various signaling pathways in a synergistic or additive manner. Vitamin K is an essential nutrient and has recently been investigated as a potential anticancer agent. The combination of Vitamin K analogs, such as vitamins K1, K2, K3, and K5, with other chemotherapeutic drugs have demonstrated a safe, cost-effective, and most efficient way to overcome drug resistance and improved the outcomes of prevailing chemotherapy. Published reports have shown that Vitamin K in combination therapy improved the efficacy of clinical drugs by promoting apoptosis and cell cycle arrest and overcoming drug resistance by inhibiting P-glycoprotein. In this review, we discuss the mechanism, cellular targets, and possible ways to develop Vitamin K subtypes into effective cancer chemosensitizers. Finally, this review will provide a scientific basis for exploiting Vitamin K as a potential agent to improve the efficacy of chemotherapeutic drugs.