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    Calcitriol (1,25-Dihydroxyvitamin D3)
    Calcitriol (1,25-Dihydroxyvitamin D3)

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    This product is for research use only, not for human use. We do not sell to patients.
    Number: - + Pieces(InventoryPieces)
    InvivoChem Cat #: V1857
    CAS #: 32222-06-3Purity ≥98%

    Description: Calcitriol (RO215535, Topitriol; 1,25(OH)2D3) is the metabolically/hormonally active form of vitamin D and a vitamin D receptor (VDR) agonist. Calcitriol is converted to metabolites more potent and rapidly acting than other forms of Vitamin D. Calcitriol has played an important role in mineral and skeletal homeostasis by regulating the differentiation, growth and the function of the cell immune system. In vitro studies, Calcitriol has been reported to dose-dependently inhibit the production of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in human peripheral blood cells (PBMC) stimulated by LPS. 

    References: J Clin Invest. 1984 Oct;74(4):1451-5; J Biol Chem. 1997 May 2;272(18):11902-7.

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    Molecular Weight (MW)416.64 
    CAS No.32222-06-3 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 83 mg/mL (199.2 mM)
    Water: <1 mg/mL
    Ethanol: 83 mg/mL (199.2 mM)
    Other info

    Chemical Name: 1α,25-Dihydroxyvitamin D3


    InChi Code: InChI=1S/C27H44O3/c1-18(8-6-14-26(3,4)30)23-12-13-24-20(9-7-15-27(23,24)5)10-11-21-16-22(28)17-25(29)19(21)2/h10-11,18,22-25,28-30H,2,6-9,12-17H2,1,3-5H3/b20-10+,21-11-/t18-,22-,23-,24?,25-,27-/m1/s1

    SMILES Code: O[[email protected]](C/C1=C/C=C2C3CC[[email protected]@H]([[email protected]]3(CCC/2)C)[[email protected]](C)CCCC(C)(O)C)C[[email protected]@H](O)C1=C

    Synonyms1,25(OH)2D3; 1,25(OH)2-D3; 1,25(OH)2-VD3; 1,25-Dihydroxyvitamin D3; RO215535, Topitriol; Rocaltrol; Calcijex; Topitriol; Silkis; Soltriol; 1α,25-Dihydroxyvitamin D3; 1α,25(OH)2D3

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    In Vitro

    In vitro activity: Calcitriol is a potent inhibitor of PHA-induced lymphocyte proliferation, achieving 70% inhibition of tritiated thymidine incorporation after 72 h in culture. Calcitriol suppresses interleukin-2 (IL-2) production by PHA-stimulated peripheral blood mononuclear cells in a concentration-dependent fashion. Calcitriol increases the concentration of intracellular calcium ([Ca2+]i) within 5 s by mobilizing calcium from the endoplasmic reticulum and the formation of inositol 1,4, 5-trisphosphate and diacylglycerol. Calcitriol can inhibit the proliferation and promote the differentiation of human prostate adenocarcinoma cells. Calcitriol causes a selective decrease in the secreted levels of type IV collagenases (MMP-2 and MMP-9). Calcitriol has antiproliferative activity in squamous cell carcinoma and prostatic adenocarcinoma and enhances the antitumor activity of platinum-based agents. Calcitriol prior to paclitaxel significantly reduces clonogenic survival compared with either agent alone in the murine squamous cell carcinoma and PC-3 cells. Calcitriol is a potent anti-proliferative agent in a wide variety of malignant cell types. Calcitriol effects are associated with an increase in G0/G1 arrest, induction of apoptosis and differentiation, modulation of expression of growth factor receptors. Calcitriol potentiates the antitumor effects of many cytotoxic agents and inhibits motility and invasiveness of tumor cells and formation of new blood vessels.

    Cell Assay: HeLa S3 cells are plated at a density of 1,000 cells/well in 96-well plates of Dulbecco’s modified Eagle’s medium (DMEM) with 10% fetal bovine serum (FBS), treated with 1% ethanol (control) or various concentrations of Calcitriol (100, 200, and 500 nM) for 72 h. A Cell Counting Kit8 (CCK-8) is used to determine cell proliferation. At 24, 48, 72, 96, 120, and 144 h after culturing with 200 nM Calcitriol, cells are harvested for analysis. Three independent experiments are performed in quadruplicate

    In VivoChronic treatment with Calcitriol (150 ng/kg per day for 4.5 months) improves the relaxations (pD2: 6.30±0.09, Emax: 68.6±3.9% in Calcitriol-treated OVX, n=8). Renal blood flow in OVX rats is reduced in both kidneys, and the flow is restored by Calcitriol treatment. The increased expression of COX-2 and Thromboxane-prostanoid (TP) receptor in OVX rat renal arteries is reduced by chronic calcitriol administration[3]. High- and low-dose Calcitriol treatment significantly decreases the systolic blood pressure (SBP) in the fructose-fed rats by 14±4 and 9±4 mmHg, respectively, at Day 56. High-dose Calcitriol treatment (20 ng/kg per day) significantly increases serum ionized calcium level (1.44±0.05 mmol/L) compare with the other groups.
    Animal modelAdult female Sprague-Dawley rats
    Formulation & Dosage150 ng/kg daily, oral gavage 
    ReferencesJ Clin Invest. 1984 Oct;74(4):1451-5; J Biol Chem. 1997 May 2;272(18):11902-7; Cancer Epidemiol Biomarkers Prev. 1997 Sep;6(9):727-32. 

    These protocols are for reference only. InvivoChem does not independently validate these methods.


    Calcipotriol induced ERα expression in ER-negative breast cancer cells.


    Calcitriol induced ERα protein expression.  2014 Mar 29;14:230. doi: 10.1186/1471-2407-14-230.


    Immunocytochemical analysis of ERα and VDR in primary and established breast cancer cells.  2014 Mar 29;14:230. doi: 10.1186/1471-2407-14-230.


    Calcitriol induced a fully active ERα.   2014 Mar 29;14:230. doi: 10.1186/1471-2407-14-230.


    Calcitriol induced ERα mRNA expression through the VDR in ERα-negative breast cancer cells.  2014 Mar 29;14:230. doi: 10.1186/1471-2407-14-230.


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