Calcitroic acid

Calcitroic acid (up to 150 μM; 30 min) potently inhibits VDR-LBD interaction with SRC2-3 coactivator peptide in a cell-free system with an IC₅₀ of 2.29 μM, but does not act as an agonist for this interaction^[1].
Calcitroic acid (up to 150 μM; 16 h) activates VDR-mediated recruitment of SRC1 in HEK-293T cells with an EC₅₀ of 0.87 μM and 55% efficacy relative to 10 nM 1,25(OH)₂D₃^[1].
Calcitroic acid (up to 150 μM; 18 h) is non-toxic to HEK-293T cells at concentrations up to 150 μM, with an LD₅₀ >100 μM^[1].
Calcitroic acid (7.5 μM; 18 h) induces VDR-mediated CYP24A1 gene expression in DU145 prostate cancer cells when administered at 7.5 μM for 18 hours^[1].
Calcitroic acid binds to VDR LBD in an agonistic conformation that supports coactivator peptide recruitment, with hydrogen bonding interactions largely matching those of 1,25(OH)₂D₃ except for the absence of a His333 interaction^[2].
Calcitroic acid (18 h) acts as a VDR agonist in HEK293 cells with an EC₅₀ of 2.89 μM, and its apparent antagonistic activity in the presence of 1,25(OH)₂D₃ is due to cytotoxicity rather than receptor antagonism^[2].
Calcitroic acid (1-50 μM; 16 h for LXRα/β, RARα assays) selectively activates the vitamin D receptor and does not interact with 14 other tested nuclear receptors at concentrations up to 50 μM^[2].
Calcitroic acid (10 μM; 18 h) upregulates the VDR target gene CYP24A1 in Caco2 cells with similar efficacy as 20 nM 1,25(OH)₂D₃, confirming its activity as a full VDR agonist^[2].
Calcitroic acid (1 h) is stable against phase I oxidative metabolism by human and mouse liver microsomes, confirming it is the true end product of the vitamin D 25-oxidative pathway^[3].
Calcitroic acid (10 μM; 2 h) is stable against phase II glucuronidation by human and mouse liver microsomes, suggesting it does not undergo this conjugation pathway in hepatic tissue^[3].
Calcitroic acid (1 h) binds to recombinant vitamin D receptor ligand-binding domain with an IC₅₀ of 8.5 μM, competing with the agonist LG190178 (HY-117182)^[4].
Calcitroic acid (16 h) acts as a partial agonist/antagonist of vitamin D receptor-mediated transcription in HEK293T cells, with an EC₅₀ of 2.5 μM for agonism and an IC₅₀ of 3.2 μM for antagonism in the presence of calcitriol^[4].
Calcitroic acid (6 μM; 24 hours) specifically upregulates CYP3A4 mRNA expression in Caco2 human colon cancer cells^[4].
Calcitroic acid (10 μM; 24 hours) upregulates both CYP3A4 and CYP24A1 mRNA expression in HIEC-6 human normal intestinal epithelial cells^[4].
Calcitroic acid (20 μM; 0-120 minutes) is stable to phase I metabolism by human liver microsomes over 2 hours and does not inhibit Calcitriol (HY-10002) metabolism^[4].
Calcitroic acid (1.40 μM; 96 h) is identified as a major terminal water-soluble metabolite produced from 1α,25-(OH)₂D₂ metabolism in human HPK1A-ras keratinocyte cells, confirmed via chromatographic comigration and mass spectral matching^[6].
Calcitroic acid (5-20 μM; 18 h) reduces nitric oxide production, pro-inflammatory gene transcription, and IL-1β protein secretion in IFNγ/LPS-activated RAW264.7 macrophages, with anti-inflammatory effects similar to 20 nM 1,25(OH)₂D₃ and no cytotoxicity in this cell line^[2].
Calcitroic acid (20 μM; 18 h) reduces nitric oxide production in IFNγ- and LPS-stimulated RAW264.7 murine macrophages, indicating anti-inflammatory activity^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.