Falecalcitriol
(Synonyms: 氟骨三醇) 目录号 : GC36026
Falecalcitriol(Fulstan; Hornel)是骨化三醇类似物，在体内有更高更长久的活性。
Cas No.:83805-11-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Falecalcitriol(Fulstan; Hornel) is an analog of calcitriol; has a higher potency both in vivo and in vitro systems, and longer duration of action in vivo.
[1]. Ito H, Ogata H, Yamamoto M, Takahashi K, Shishido K, Takahashi J, Taguchi S, Kinugasa E. Comparison of oral falecalcitriol and intravenous calcitriol in hemodialysis patients with secondary hyperparathyroidism: a randomized, crossover trial. Clin Nephro [2]. Tokunaga M, Tamura M, Kabashima N, Serino R, Shibata T, Matsumoto M, Miyamoto T, Miyazaki M, Furuno Y, Takeuchi M, Abe H, Okazaki M, Otsuji Y. Falecalcitriol for conventional vitamin D therapy-resistant secondary hyperparathyroidism in a continuous ambul [3]. Iwao Y, Yamaguchi Y, Fujii K, Toba Y, Asada M, Nagano N, Yamamoto H, Hyoma K, Yamada S, Hirano H, Tone Y, Ohtani H, Saika Y, Fujii R. Long-term suppressive effect of falecalcitriol on parathyroid hormone secretion in secondary hyperparathyroidism in hemo [4]. Morii H. Falecalcitriol as a new therapeutic agent for secondary hyperparathyroidismClin Calcium. 2005 Jan;15(1):29-33. [5]. Ohtsuka N, Urayama K. Pharmacological action and clinical effects of falecalcitriol, a highly potent derivative of active vitamin D3.Nihon Yakurigaku Zasshi. 2002 Dec;120(6):427-36. [6]. Jean-Pierre BÉguÉ, DaniÈle Bonnet-Delpon.Recent advances (1995-2005) in fluorinated pharmaceuticals based on natural products. Journal of Fluorine Chemistry.Volume 127, Issue 8, August 2006, Pages 992-1012
| Cas No. | 83805-11-2 | SDF | |
| 别名 | 氟骨三醇 | ||
| Canonical SMILES | C[C@]([C@]/12[H])([C@H](CC2)[C@@H](CCCC(C(F)(F)F)(C(F)(F)F)O)C)CCCC1=C/C=C(C[C@@H](O)C[C@@H]3O)\C3=C | ||
| 分子式 | C27H38F6O3 | 分子量 | 524.58 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C,unstable in solution, ready to use. |
| 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。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.9063 mL | 9.5314 mL | 19.0629 mL |
| 5 mM | 0.3813 mL | 1.9063 mL | 3.8126 mL |
| 10 mM | 0.1906 mL | 0.9531 mL | 1.9063 mL |
| 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。
[Pharmacological action and clinical effects of Falecalcitriol, a highly potent derivative of active vitamin D3]
Nihon Yakurigaku Zasshi 2002 Dec;120(6):427-36.PMID:12528474DOI:10.1254/fpj.120.427.
Much effort has been made to create highly potentiated active vitamin D for better clinical applications and Falecalcitriol was successfully synthesized as one of such candidates with highly potent and long-lasting effects. Its chemical structure has a calcitriol side chain modification in which both methyls at positions C-26 and C-27 are substituted by tri-fluoromethyls. The mechanism for its strong and long-lasting effects is probably due to altered side chain metabolism and decreased inactivation. Although C-24 position hydroxylation catalyzed by Cyp24 inactivates calcitriol, falecarcitriol is metabolized to C-23S hydroxylated metabolite by the same enzyme Cyp24 and this metabolite still has strong activity. Stronger action of Falecalcitriol has been shown in target organs or cells of active vitamin D such as bone, parathyroid cells, and keratinocytes, when compared with calcitriol, the endogenous active form of vitamin D. Daily oral administration of Falecalcitriol at doses lower than those required for calcitriol has been shown to have clinical effects for the treatment of diseases such as hyperparathyroidism due to chronic renal failure (2 degrees HPT), rickets, osteomalacia and hypoparathyroidism. The comparative study with alfacalcidol showed its specific action on parathyroid hormone suppression and better improvement of bone metabolism markers in 2 degrees HPT patients.
[Falecalcitriol as a new therapeutic agent for secondary hyperparathyroidism]
Clin Calcium 2005 Jan;15(1):29-33.PMID:15632470doi
The 26 and 27 positions of vitamin D molecular structure of calcitriol were fluorinated with 3 atoms of fluorine each and the new compound was named Falecalcitriol (F6). This new compound was found to be 10 to 100 times more active compared with calcitriol depending on the target organs. As a mechanism of strong action of F6 it was discovered that F6 is hydroxylated at 23 position which has almost the same activity as the mother compound. It was also demonstrated that the PTH suppressive effect was relatively stronger than the calcium absorption action from the intestine. Thus F6 was authorized to be applied to the treatment of secondary hyperparathyoroidism in hemodialysed patients as well as to the treatment of hypoparathyroidism.
Comparison of oral Falecalcitriol and intravenous calcitriol in hemodialysis patients with secondary hyperparathyroidism: a randomized, crossover trial
Clin Nephrol 2009 Jun;71(6):660-8.PMID:19473635DOI:10.5414/cnp71660.
Background: Falecalcitriol is a novel vitamin D analog, which has a greater potential to suppress parathyroid hormone (PTH) and a longer half-life. There are few studies to compare clinical effects of oral Falecalcitriol treatment with those of intravenous calcitriol treatment. Methods: Twenty-one patients with moderate to severe SHPT were included in a random 2 x 2 crossover trial with the two vitamin D analogs (12 weeks for each treatment). The primary endpoint measure was a decrease in serum intact PTH (iPTH) level, and the secondary outcome measures included changes in serum calcium (Ca), phosphate (P), and metabolic bone marker levels. Results: Both treatments decreased iPTH and whole PTH (wPTH) levels by similar degrees (iPTH, -200.1 +/- 107.0 with Falecalcitriol vs. -200.8 +/- 114.9 pg/ml with calcitriol, p = 0.9895; wPTH, -137.1 +/- 73.1 with Falecalcitriol vs. -120.4 +/- 81.1 pg/ml with calcitriol, p = 0.5603). Serum Ca, P, and Ca x P product levels at the end of each treatment were comparable and the frequencies of hypercalcemia and hyperphosphatemia were also similar during each treatment period. Although intravenous calcitriol treatment significantly changed intact osteocalcin and cross-linked N-telopeptide of type I collagen after 12 weeks, oral Falecalcitriol treatment did not change any bone metabolic marker level. Conclusion: The present study showed that oral Falecalcitriol treatment is effective for PTH suppression, and Ca and P metabolism in hemodialysis patients with moderate to severe SHPT, as well as intravenous calcitriol administration.
Controlled trial of Falecalcitriol versus alfacalcidol in suppression of parathyroid hormone in hemodialysis patients with secondary hyperparathyroidism
Am J Kidney Dis 1998 Aug;32(2):238-46.PMID:9708607DOI:10.1053/ajkd.1998.v32.pm9708607.
Active vitamin D3 is extensively used for the treatment of secondary hyperparathyroidism in hemodialysis patients. But it is often impossible to administer enough dose to suppress parathyroid hormone (PTH) level, because of hypercalcemia and hyperphosphatemia. New modalities with higher specificity for PTH suppression are desirable. We conducted a crossover comparative study of Falecalcitriol, an active vitamin D3 analog, and alfacalcidol (1alpha[OH]D3). In this study, 25 hemodialysis patients with moderate to severe secondary hyperparathyroidism who had normal serum calcium levels were enrolled. They received daily oral doses of alfacalcidol during an 8-week observation period. Based on serum calcium levels and intact PTH, the subjects were allocated into two groups, and a comparative study was conducted using unmasked crossover design of two drugs x two periods. The dosage of both drugs was adjusted to maintain the initial serum calcium levels, and the relative change (%change) of serum biochemical parameters were compared. Comparison of two drugs in period 1 was taken as primary efficacy evaluation. Reproducibility of drug action was confirmed by comparing the effect of Falecalcitriol between period 1 and 2. The percent change of PTH of Falecalcitriol was lower than that of alfacalcidol: Those were, respectively, -7.89% and +30.42% for c-terminal PTH (P = 0.022), -4.39% and +38.88% for i-PTH (P = 0.077), and +3.68% and +30.52% for midregion PTH (P = 0.099). The similar changes were observed in the Falecalcitriol group during period 2, confirming the reproducibility. Falecalcitriol was found to be superior to alfacalcidol in suppression of PTH levels in patients with moderate to severe secondary hyperparathyroidism when it is administered in equivalent doses that might maintain similar serum calcium levels.
Recent developments for introducing a hexafluoroisopropanol unit into the Vitamin D side chain
J Steroid Biochem Mol Biol 2018 Mar;177:250-254.PMID:28716761DOI:10.1016/j.jsbmb.2017.07.008.
Among numerous studies on synthetic approaches to and the biological activities of vitamin D analogues, we herein focused on Falecalcitriol, an analogue of calcitriol (1α,25-dihydroxyvitamin D3), in which a 26,26,26,27,27,27-hexafluoroisopropanol unit has been introduced into the side chain. Falecalcitriol was designed to escape from the metabolism of CYP24A1 and has been used as a drug to treat secondary hyperparathyroidism since 2001. Its metabolite, the 23-hydroxy form, retains biological activity and resistants to further metabolism. Recent developments in synthetic methodologies for introducing the hexafluoroisopropanol unit into the vitamin D CD-ring side chain were described herein.