• CAT Number: I004076
  • CAS Number: 55721-11-4
  • Molecular Formula: C27H44O3
  • Molecular Weight: 416.64
  • Purity: ≥95%
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<p style=/line-height:25px/>Secalciferol is a metabolite of Vitamin D, a possibly anti-inflammatory steroid which is involved in bone ossification.<br>IC50 value:<br>Target:<br>In addition, it is known that Secalciferol mediates calcium and phosphorus homeostasis. Also Secalciferol inhibits calcium channels in osteosarcoma cells via suppressing the effects of 1α, 25-dihydroxyvitamin D3 and testosterone. Alternate studies indicate that Secalciferol can decrease the abundance of p53 and Pi-induced cytochrome c translocation. Furthermore, Secalciferol can increase cell proliferation in resting zone (RC) chondrocytes and inhibits matrix enzymes by possibly inhibiting the degradation of the matrix.</p>

Catalog Number I004076
CAS Number 55721-11-4


Molecular Formula


Purity 95%
Target VD/VDR
Solubility 10 mM in DMSO
Storage Store at -20°C

<p style=/line-height:25px/>
<br>[1]. Rubin LP, Yeung B, Vouros P et al. Evidence for human placental synthesis of 24,25-dihydroxyvitamin D3 and 23,25-dihydroxyvitamin D3. Pediatr Res. 1993 Jul;34(1):98-104.
The two principal dihydroxylated metabolites of the vitamin D prohormone 25-hydroxyvitamin D3 [25(OH)D3] are 1 alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3, the active hormone] and 24R,25-dihydroxyvitamin D3 [24,25(OH)2D3, a putative regulator of developmental bone formation]. Although several studies have demonstrated placental synthesis of 1,25(OH)2D3 from 25(OH)D3, placental production of 24,25(OH)2D3 has not been thoroughly investigated. Therefore, we studied 25(OH)D3 metabolism in term human placenta using a villous explant model and cultures of isolated trophoblast and villous mesenchymal cells. We determined that both vitamin D-replete and vitamin D-deficient trophoblast metabolize 25(OH)D3 predominantly via 24-hydroxylation. Placental 24,25(OH)2D3 was identified by cochromatography with authentic standard on four different HPLC systems, scanning UV spectrophotometry profile of the metabolite, sensitivity to periodate cleavage, and mass spectrometry of the putative placental 24,25(OH)2D3 and its periodate cleavage product. We also identified for the first time placental synthesis of 23,25(OH)2D3 using cochromatography with authentic standard on two different HPLC systems, scanning UV spectrophotometry, resistance to periodate cleavage, and mass spectrometry. When trophoblast was incubated for up to 4 h with physiologic concentrations of [3H]25(OH)D3 (6 nM) significant amounts of [3H]24,25(OH)2D3 were produced, but [3H]1,25(OH)2D3 could not be consistently detected. In contrast, when we incubated trophoblast with supraphysiologic concentrations of 25(OH)D3 (6-10 microM), both 24,25(OH)2D3 and 1,25(OH)2D3 were synthesized. These results provide unequivocal evidence for placental synthesis of both 24,25(OH)2D3 and 23,25(OH)2D3.
<br>[2]. Yamamoto T, Ozono K, Shima M, et al. 24R,25-dihydroxyvitamin D3 increases cyclic GMP contents, leading to an enhancement of osteocalcin synthesis by 1,25-dihydroxyvitamin D3 in cultured human osteoblastic cells. Exp Cell Res. 1998 Oct 10;244(1):71-6.
<br>[3]. Sakaki T, Sawada N, Takeyama K, et al. Enzymatic properties of mouse 25-hydroxyvitamin D3 1 α-hydroxylase expressed in Escherichia coli. Eur J Biochem. 1999 Feb;259(3):731-8.
<br>[4]. Norman AW, Okamura WH, Bishop JE, Henry HL. Update on biological actions of 1α,25(OH)2-vitamin D3 (rapid effects) and 24R,25(OH)2-vitamin D3. Mol Cell Endocrinol. 2002 Nov 29;197(1-2):1-13
<br>[5]. Hurst-Kennedy J, Zhong M, Gupta V et al. 24R,25-Dihydroxyvitamin D3, lysophosphatidic acid, and p53: a signaling axis in the inhibition of phosphate-induced chondrocyte apoptosis. J Steroid Biochem Mol Biol. 2010 Oct;122(4):264-71.
<br>[6]. Wehmeier KR, Alamir AR, Sultan S, et al. 24, 25-dihydroxycholecalciferol but not 25-hydroxycholecalciferol suppresses apolipoprotein A-I gene expression. Life Sci. 2011 Jan 3;88(1-2):110-6.

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