Info: Read More
  • 中药标准品生产商,产品定制服务
  • 维生素D2

    Ergocalciferol

    维生素D2
    产品编号 CFN90049
    CAS编号 50-14-6
    分子式 = 分子量 C28H44O = 396.65
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Miscellaneous
    植物来源 From the edible mushroom Cantharelluscibarius (chanterelle).
    ChemFaces的产品在影响因子大于5的优秀和顶级科学期刊中被引用
    提供自定义包装
    产品名称 产品编号 CAS编号 包装 QQ客服
    维生素D2 CFN90049 50-14-6 10mg QQ客服:2056216494
    维生素D2 CFN90049 50-14-6 20mg QQ客服:2056216494
    维生素D2 CFN90049 50-14-6 50mg QQ客服:2056216494
    维生素D2 CFN90049 50-14-6 100mg QQ客服:2056216494
    存储与注意事项
    1. 在您收到产品后请检查产品。如无问题,请将产品存入冰霜并且样品瓶保持密封,产品可以存放长达24个月(2-8摄氏度)。

    2. 只要有可能,产品溶解后,您应该在同一天应用于您的实验。 但是,如果您需要提前做预实验,或者需要全部溶解,我们建议您将溶液以等分试样的形式存放在-20℃的密封小瓶中。 通常,这些可用于长达两周。 使用前,打开样品瓶前,我们建议您将产品平衡至室温至少1小时。

    3. 需要更多关于溶解度,使用和处理的建议? 请发送电子邮件至:service@chemfaces.com
    订购流程
  • 1. 在线订购
  • 请联系我们QQ客服

  • 2. 电话订购
  • 请拨打电话:
    027-84237683 或 027-84237783

  • 3. 邮件或传真订购
  • 发送电子邮件到: manager@chemfaces.com 或
    发送传真到:027-84254680

  • 提供订购信息
  • 为了方便客户的订购,请需要订购ChemFaces产品的客户,在下单的时候请提供下列信息,以供我们快速为您建立发货信息。
  •  
  • 1. 产品编号(CAS No.或产品名称)
  • 2. 发货地址
  • 3. 联系方法 (联系人,电话)
  • 4. 开票抬头 (如果需要发票的客户)
  • 5. 发票地址(发货地址与发票地址不同)
  • 发货时间
    1. 付款方式为100%预付款客户,我们将在确认收到货款后当天或1-3个工作日发货。

    2. 付款方式为月结的客户,我们承诺在收到订单后当天或1-3个工作日内发货。

    3. 如果客户所需要的产品,需要重新生产,我们有权告知客户,交货时间需要延期。
    ChemFaces的产品在许多优秀和顶级科学期刊中被引用

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.
    IF=36.216(2019)

    PMID: 29328914

    Cell Metab. 2020 Mar 3;31(3):534-548.e5.
    doi: 10.1016/j.cmet.2020.01.002.
    IF=22.415(2019)

    PMID: 32004475

    Mol Cell. 2017 Nov 16;68(4):673-685.e6.
    doi: 10.1016/j.molcel.2017.10.022.
    IF=14.548(2019)

    PMID: 29149595

    ACS Nano. 2018 Apr 24;12(4): 3385-3396.
    doi: 10.1021/acsnano.7b08969.
    IF=13.903(2019)

    PMID: 29553709

    Nature Plants. 2016 Dec 22;3: 16206.
    doi: 10.1038/nplants.2016.205.
    IF=13.297(2019)

    PMID: 28005066

    Sci Adv. 2018 Oct 24;4(10): eaat6994.
    doi: 10.1126/sciadv.aat6994.
    IF=12.804(2019)

    PMID: 30417089
    我们的产品现已经出口到下面的研究机构与大学,并且还在增涨
  • University of Maryland School of Medicine (USA)
  • Lund University (Sweden)
  • The Vancouver Prostate Centre (VPC) (Canada)
  • Julius Kühn-Institut (Germany)
  • Universidad Miguel Hernández (Spain)
  • Institute of Tropical Disease Universitas Airlangga (Indonesia)
  • Gyeongsang National University (Korea)
  • Instituto de Investigaciones Agropecuarias (Chile)
  • University of Stirling (United Kingdom)
  • Indian Institute of Science (India)
  • Heidelberg University (Germany)
  • Universiti Sains Malaysia (Malaysia)
  • Sapienza University of Rome (Italy)
  • University of Otago (New Zealand)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • iScience.2020, 23(2):100849.
  • Int. J. Mol. Sci. 2022, 23(3),1696.
  • Int J Mol Sci.2017, 18(12)
  • Front Pharmacol.2020, 11:683.
  • Horticulture Research2022, uhac276.
  • J. Soc. Cosmet. Sci. Korea2016, 163-171
  • Appl. Sci.2020, 10(23), 8729
  • Molecules.2020, 25(15):3353.
  • Vietnam J. Chemistry2022, 60(2):211-222
  • Antioxidants (Basel).2020, 9(6):466.
  • J Phys Chem Lett.2021, 12(7):1793-1802.
  • J Biol Chem.2014, 289(3):1723-31
  • Int J Pharm.2022, 618:121636.
  • Planta Med.2022, a-1876-3009.
  • Biomolecules.2020, 10(2):E184
  • UDC.2020, 19(4).
  • Pharmacol Res.2020, 161:105205.
  • Molecules.2022, 27(13):4227.
  • Invest New Drugs.2017, 35(2):166-179
  • J. Food Composition and Anal.2022, V 109:104482.
  • J Nat Prod.2015, 78(6):1339-4
  • Molecules.2018, 23(11):E2837
  • Food Analytical Methods2020, 1-10
  • ...
  • 生物活性
    Description: Ergocalciferol (Vitamin D2) is a selective inhibitor of mammalian DNA polymerase A (pol A) with IC50 of 123 mM. Ergocalciferol can delay the development of secondary hyperparathyroidism in children with CKD2-3. Ergocalciferol can cause HL-60 apoptosis via a modulation of mitochondria involving ROS production, GSH depletion, caspase activation, and Fas induction, on the basis of anticancer activity of ergocalciferol, it may be feasible to develop chemopreventive agents from edible mushrooms or hop. Ergocalciferol can prevent glucocorticoid-induced bone loss, but even increase lumbar spine and femoral neck bone mineral densities (BMD) in postmenopausal women commencing glucocorticoid therapy, it also is safe and effective in reducing the risk of a fracture in elderly patients with AD.
    Targets: IL Receptor | Caspase | ROS | DNA polymerase A | GSH | Fas | PARP
    In vivo:
    Clin J Am Soc Nephrol. 2012 Feb;7(2):216-23.
    Ergocalciferol supplementation in children with CKD delays the onset of secondary hyperparathyroidism: a randomized trial.[Pubmed: 22266572 ]
    Vitamin D deficiency is an important contributor to the development of hyperparathyroidism and is independently associated with cardiovascular and bone disease. The hypothesis was that nutritional vitamin D (ergocalciferol) supplementation in children with CKD stages 2-4 delays the onset of secondary hyperparathyroidism.
    METHODS AND RESULTS:
    A randomized, double-blinded, placebo-controlled study in children with CKD2-4 who had 25-hydroxyvitamin D [25(OH)D] deficiency was conducted. Ergocalciferol (or a matched placebo) was given daily as per Kidney Disease Outcomes Quality Initiative guidelines. The primary endpoint was the time to development of hyperparathyroidism. Seventy-two children were screened. Forty-seven children were 25(OH)D-deficient and randomly assigned to receive ergocalciferol or placebo. Twenty children in each arm completed the study; median follow-up was 12 months. Groups were well matched for age, race, estimated GFR, and season when recruited. Nine of 20 children on placebo and 3 of 20 children on ergocalciferol developed hyperparathyroidism (odds ratio, 4.64; 95% confidence interval, 1.02-21.00). The time to development of hyperparathyroidism was significantly longer with ergocalciferol treatment compared with placebo (hazard ratio, 0.30; 95% confidence interval, 0.09-0.93, P=0.05). With ergocalciferol treatment, normal 25(OH)D levels were achieved in all 8 children with CKD2, 8 of 11 children with CKD3, but not in the single patient with CKD4. There were no ergocalciferol-related adverse events. 25(OH)D levels >100 nmol/L were required to achieve normal levels of 1,25-dihydroxyvitamin D.
    CONCLUSIONS:
    Ergocalciferol is an effective treatment that delays the development of secondary hyperparathyroidism in children with CKD2-3.
    Pediatr Nephrol. 2013 Aug;28(8):1261-6.
    Ergocalciferol decreases erythropoietin resistance in children with chronic kidney disease stage 5.[Pubmed: 23420502]
    Vitamin D(Ergocalciferol) insufficiency is related to erythropoietin resistance in chronic kidney disease (CKD). This study was conducted to evaluate the effect of ergocalciferol on the dose of erythrocyte-stimulating agent (ESA) administered to children with CKD stage 5 and vitamin D insufficiency.
    METHODS AND RESULTS:
    Twenty patients aged <18 years with CKD stages 5 or 5D and vitamin D insufficiency were divided into two groups. During the 12-week study, ten patients received oral ergocalciferol (treatment) whereas the other ten patients did not (control). The ESA dosage was recorded monthly. There were no significant differences in demographic data, ESA dosages, and laboratory data, including corrected calcium, phosphorus, parathyroid hormone, hemoglobin, ferritin, 25-hydroxyvitamin D (25D), and transferrin saturation levels, between the two groups at baseline. At the completion of the study, serum 25D levels in the treatment group were significantly increased from baseline (p = 0.02) and were significantly higher than the serum 25D levels in the controls (p < 0.005). The ESA dosage in the treatment group was significantly decreased when compared to baseline (p = 0.04).
    CONCLUSIONS:
    Vitamin D deficiency should be routinely detected and treated. Our results show that the administration of ergocalciferol in conjunction with 1,25-dihydroxyvitamin D3 reduced the dose of ESA required to treat children with CKD stages 5 and 5D and may decrease erythropoietin resistance.
    Scand J Clin Lab Invest. 2013 Mar;73(2):107-16.
    Ergocalciferol treatment and aspects of mineral homeostasis in patients with chronic kidney disease stage 4-5.[Pubmed: 23281842]
    Focus on non-classical effects and possible less side effects of treatment with nutritional vitamin D, raises the expectation of possible benefits from treating chronic kidney disease (CKD) patients with ergocalciferol (vitamin D2). Treatment with 1,25(OH)2 vitamin D (calcitriol) induces elevated fibroblast growth factor 23 (FGF23), while epidemiological studies have found positive effects of nutritional and 25(OH)vitamin D on mortality in CKD. Disturbed mineral homeostasis in CKD is correlated to adverse outcome and cardiovascular mortality. The objective was to examine the possible effects of treatment with high doses of ergocalciferol on parameters of mineral homeostasis in predialysis CKD patients.
    METHODS AND RESULTS:
    A total of 43 adult patients with CKD stage 4-5, not receiving vitamin D supplementation, were studied, and allocated by simple randomization to either an intervention (n = 26) or a control group (n = 17). The intervention group received ergocalciferol, 50.000 IU/week for 6 weeks. Plasma FGF23, creatinine, parathyroid hormone (PTH), phosphate and ionized calcium were obtained at baseline and after the 6 weeks. The intervention group had a significant increase in 25(OH)D2 concentration from < 10 to 90 ± 4 nmol/L, while 1,25(OH)2D (62 ± 6 at baseline and 67 ± 6 pmol/L at 6 weeks) remained stable. No changes were seen in the circulating vitamin D concentrations in the control group. After the 6 weeks of treatment no significant changes were seen in concentration of creatinine, phosphate, ionized calcium, PTH and FGF23 remained stable.
    CONCLUSIONS:
    No harmful effects of short-term treatment with high-dose ergocalciferol were observed on markers of mineral homeostasis and FGF23 in CKD patients stage 4-5.
    Am J Med. 1995 May;98(5):459-63.
    Cyclical etidronate plus ergocalciferol prevents glucocorticoid-induced bone loss in postmenopausal women.[Pubmed: 7733124]
    The two groups did not differ with respect to age, years since the menopause, mean daily To assess the benefit of cyclical etidronate plus ergocalciferol for the prevention of glucocorticoid-induced bone loss in a 2-year, prospective, open study based in an osteoporosis clinic.
    METHODS AND RESULTS:
    Group 1 consisted of 15 postmenopausal women (mean age 62.6 +/- 3.3 years) who commenced glucocorticoid therapy and were treated with cyclical etidronate (400 mg/d for the first month; thereafter, 400 mg/d for 2 weeks of every 3-month period), elemental calcium (1 g/d), and ergocalciferol (0.5 mg/wk). Group 2 consisted of 11 postmenopausal women (mean age 60.2 +/- 4.7 years) with glucocorticoid-induced osteoporosis, who were attending the clinic at the same time and were treated with calcium supplements only (1 g/d). Lumbar spine and femoral neck bone mineral densities (BMD) were measured at baseline and after 12 and 24 months of glucocorticoid therapy using a dual energy x-ray absorptiometer. The two groups did not differ with respect to age, years since the menopause, mean daily glucocorticoid dose, and baseline BMD values. During the first year of therapy, mean lumbar spine BMD increased from an initial value of 0.88 g/cm2 to 0.94 g/cm2, an increase of 7% per year (95% confidence interval [CI] 3.7% to 10.2%; P < 0.001 compared with controls). Significant increases in BMD of 2.5% per year were also observed in the femoral neck (95% CI -1% to 6%; P < 0.01 compared with controls). After the second year of cyclical etidronate therapy, femoral neck BMD continued to increase (P < 0.05 compared with value at 12 months), while lumbar spine BMD remained stable.
    CONCLUSIONS:
    Chronic glucocorticoid therapy may result in bone loss at most skeletal sites. Therapy with cyclical etidronate plus ergocalciferol not only prevented glucocorticoid-induced bone loss, but even increased lumbar spine and femoral neck BMD in postmenopausal women commencing glucocorticoid therapy.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.5211 mL 12.6056 mL 25.2111 mL 50.4223 mL 63.0279 mL
    5 mM 0.5042 mL 2.5211 mL 5.0422 mL 10.0845 mL 12.6056 mL
    10 mM 0.2521 mL 1.2606 mL 2.5211 mL 5.0422 mL 6.3028 mL
    50 mM 0.0504 mL 0.2521 mL 0.5042 mL 1.0084 mL 1.2606 mL
    100 mM 0.0252 mL 0.1261 mL 0.2521 mL 0.5042 mL 0.6303 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    部分图片展示
    产品名称 产品编号 CAS编号 分子式 = 分子量 位单 联系QQ
    蜕皮甾酮-20,22-单丙酮化物; Ecdysterone 20,22-monoacetonide CFN98229 22798-96-5 C30H48O7 = 520.7 5mg QQ客服:2159513211
    蜕皮甾酮2,3:20,22- 二缩丙酮; Ecdysterone 2,3:20,22-diacetonide CFN98230 22798-98-7 C33H52O7 = 560.8 5mg QQ客服:1457312923
    维生素D3; Vitamin D3 CFN90027 67-97-0 C27H44O = 384.64 20mg QQ客服:2056216494
    维生素D2; Ergocalciferol CFN90049 50-14-6 C28H44O = 396.65 20mg QQ客服:215959384
    二氢胆固醇; Dihydrocholesterol CFN90608 80-97-7 C27H48O = 388.67 20mg QQ客服:1413575084
    胆固醇; 胆甾醇; Cholesterol CFN90040 57-88-5 C27H46O = 386.67 20mg QQ客服:215959384
    4β-羟基胆固醇; 4-Beta-Hydroxycholesterol CFN90611 17320-10-4 C27H46O2 = 402.66 5mg QQ客服:3257982914
    7β-羟基胆固醇; 7Beta-Hydroxycholesterol CFN90610 566-27-8 C27H46O2 = 402.65 5mg QQ客服:2159513211
    7-酮基胆固醇; 7-Ketocholesterol CFN91812 566-28-9 C27H44O2 = 400.6 5mg QQ客服:1457312923
    7-氧胆固醇乙酯; 7-Oxocholesteryl acetate CFN91647 809-51-8 C29H46O3 = 442.7 5mg QQ客服:1457312923

    信息支持


    公司简介
    订购流程
    付款方式
    退换货政策

    ChemFaces提供的产品仅用于科学研究使用,不用于诊断或治疗程序。

    联系方式


    电机:027-84237783
    传真:027-84254680
    在线QQ: 1413575084
    E-Mail:manager@chemfaces.com

    湖北省武汉沌口经济技术开区车城南路83号1号楼第三层厂房


    ChemFaces为科学家,科研人员与企业提供快速的产品递送。我们通过瑞士SGS ISO 9001:2008质量体系认证天然化合物与对照品的研发和生产