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falecalcitriol (Fulstan / F6VD3 / falecalcitriol)

✓ Approved

Taisho Pharmaceutical Co., Ltd. · VDR · Small Molecule

What is falecalcitriol?

falecalcitriol is a small molecule developed by Taisho Pharmaceutical Co., Ltd.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesFulstan, F6VD3, falecalcitriol
CompanyTaisho Pharmaceutical Co., Ltd.
Drug ClassSmall Molecule
Molecular TargetVDR
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Taisho Pharmaceutical Co., Ltd.

Mechanism of Action

Molecular Targets

falecalcitriol acts on 1 molecular target:

VDRvitamin D receptor (NR1I1, PPP1R163)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

falecalcitriol is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Endocrine disordersHyperparathyroidism secondary✓ Approved

Related Research Articles

PubMedBiomedicines2025-04-29

Recent Advancements Towards the Use of Vitamin D Isoforms and the Development of Their Synthetic Analogues as New Therapeutics.

Patel Rajiv R, Nandini, Kharkwal Harsha H, Saha Moumita M et al.

Vitamin D and its metabolites are essential in various physiological processes, including muscle strength, metabolism, antifibrotic activity, and immune regulation. Researchers are focusing on developing vitamin D derivatives with optimized receptor selectivity and reduced systemic toxicity, enhancing their therapeutic efficacy against cancer, autoimmune disorders, and inflammatory diseases. Several analogues, such as alfacalcidol, paricalcitol, and falecalcitriol, are used for managing CKD-related bone disorders, while eldecalcitol is effective for osteoporosis, and calcipotriol against psoriasis. Recent studies have explored their impact on metabolic pathways, parathyroid hormone secretion, asthma, and liver fibrosis, revealing their broad clinical potential. Despite enormous efforts in the past decades, translations of vitamin D-drugs are disproportionately limited, mainly due to toxicity due to calcemic effects and undesirable metabolic profile. This review discusses structural modifications in vitamin D3, their influence on VDR binding, transcriptional activity, and calcium homeostasis, along with their role in targeting pathways like EGFR, KRAS, and Hedgehog in cancers. Advanced analytical techniques such as LC/ESI-MS/MS facilitate precise detection of vitamin D metabolites, further improving pharmacokinetic profiling. Future research may enable the clinical approval of novel vitamin D-based therapeutics with minimal disruption to calcium-phosphorus balance.

PMID 40299638
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PubMedJournal of pharmaceutical and biomedical analysis2020-02-12

Active vitamin D and vitamin D analogs stimulate fibroblast growth factor 23 production in osteocyte-like cells via the vitamin D receptor.

Yashiro Mitsuru M, Ohya Masaki M, Mima Toru T, Nakashima Yuri Y et al.

Osteocytes play an important role in the regulation of serum phosphorus by producing fibroblast growth factor 23 (FGF23). FGF23 production is stimulated by 1α,25-dihydroxyvitamin D in osteocytes. However, it is unclear whether vitamin D induces FGF23 production in osteocytes directly. Therefore, we investigated vitamin D-induced FGF23 production in osteocyte-like cells derived from MC3T3-E1 osteocyte progenitor cells. We also investigated differences in the induction of FGF23 by 1α,25-dihydroxyvitamin D and various vitamin D analogs. MC3T3-E1 cells were differentiated into osteocyte-like cells (MCT3-E1-OLCs) by treatment with various agents including β-glycerophosphate and ascorbic acid. MCT3-E1-OLCs were stimulated with 1α,25-dihydroxyvitamin D3 and subsequent FGF23 gene expression was 2631 ± 605 times higher compared with untreated cells. The expression of FGF23 in MCT3-E1-OLCs transfected with a knockdown sequence against vitamin D receptor (VDR) was significantly decreased compared with that in cells transfected with the control vector. Therefore, the induction of FGF23 in osteocytes by vitamin D may be primarily mediated via VDR. The potential of 25(OH)vitamin D3, paricalcitol, and maxacalcitol to induce FGF23 production was almost the same as that of 1α,25-dihydroxyvitamin D3. However, falecalcitriol and eldecalcitol demonstrated a reduced potential to induce FGF23 compared with 1α,25-dihydroxyvitamin D3. Our results demonstrate that FGF23 induction is different among the analogs of 1α,25-dihydroxyvitamin D3. Therefore, an appropriate vitamin D analog should be chosen for each patient with mineral and bone disorder, considering its effect on FGF23 production.

PMID 32045827
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PubMedThe Journal of steroid biochemistry and molecular biology2017-07-19

Recent developments for introducing a hexafluoroisopropanol unit into the Vitamin D side chain.

Kawagoe Fumihiro F, Sugiyama Toru T, Uesugi Motonari M, Kittaka Atsushi A

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.

PMID 28716761
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PubMedClinical and experimental nephrology2016-12-23

Research on kidney and mineral metabolism in Japan: past, present, and future.

Mizobuchi Masahide M, Ogata Hiroaki H, Koiwa Fumihiko F, Kinugasa Eriko E et al.

Since the identification of the kidney was the main site for the synthesis of calcitriol (1α, 25-dihydroxycholecalciferol), research on chronic kidney disease (CKD)-associated mineral metabolism disorders and their management has made rapid progress. Various active analogues of calcitriol have clinically become available for treating secondary hyperparathyroidism (SHPT), which is a representative mineral metabolism abnormality in CKD patients. A calcimimetic compound cinacalcet hydrochloride has also been developed for the medical management of SHPT through a different mechanism involving the calcium-sensing receptor. The concept of CKD-mineral and bone disorder (CKD-MBD) was proposed in 2006 to provide a comprehensive understanding of a disorder related to mineral metabolism abnormalities of CKD, based on the fact that these abnormalities are closely associated with cardiovascular disease as well as bone disorders (renal osteodystrophy). There has been a recent surge in the development of phosphate binders for CKD-MBD, focused on an effort to improve mortality. In Japan, high-quality basic and clinical research on CKD-MBD has led to the development of novel therapeutic drugs, such as maxacalcitol, falecalcitriol, and bixalomer. New practice guidelines have been published and are widely adapted in clinical practice.

PMID 28005175
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PubMedJournal of molecular endocrinology2016-05-08

Transcriptional activation of the wild-type and mutant vitamin D receptors by vitamin D3 analogs.

Futawaka Kumi K, Tagami Tetsuya T, Fukuda Yuki Y, Koyama Rie R et al.

The active form of vitamin D3 (1α,25(OH)2D3, also known as calcitriol) controls the expression of target genes via the vitamin D receptor (VDR). Vitamin D-dependent rickets type II (VDDRII) is a congenital disease caused by inactivating mutations in the VDR The condition is treated with high doses of calcitriol, but the therapeutic effects of other synthetic VD3 analogs have not yet been investigated. In the present study, we analyzed the transcriptional activity of seven different VD3 analogs with VDRs carrying ligand-binding domain mutations identified in VDDRII patients. Wild-type VDR (WT-VDR) and seven mutant VDRs were expressed in TSA201 human embryonic kidney cells, HepG2 human liver cancer cells, and MC3T3-E1 mouse calvaria cells, and their transcriptional activation with VD3 analogs were analyzed by performing transient expression assays, western blotting, and quantitative real-time PCR. The results demonstrated that falecalcitriol stimulated significantly higher transcriptional activation of the WT-VDR and some mutant VDRs than did calcitriol. Calcitriol showed almost no transcriptional activation of the VDR with the I268T mutation identified in a severe case of VDDRII, whereas falecalcitriol caused a dose-dependent increase in the activation of this mutant VDR. Our findings demonstrate that falecalcitriol has a VDR activation profile distinct from that of calcitriol and may exhibit therapeutic effects even on difficult-to-treat VDDRII cases resistant to calcitriol. It is also possible that VDDRII patients responding to high doses of calcitriol could be appropriately treated with low doses of falecalcitriol.

PMID 27154546
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PubMedPloS one2016-01-27

Effect of Vitamin D Receptor Activators on Glomerular Filtration Rate: A Meta-Analysis and Systematic Review.

Zhang Qian Q, Li Ming M, Zhang Tiansong T, Chen Jing J

Vitamin D receptor activators (VDRAs) can protect against mineral bone disease, but they are reported to elevate serum creatinine (SCr) and may also reduce glomerular filtration rate (GFR). We conducted a systematic review and meta-analysis of randomized clinical trials (RCTs) to evaluate the effect of VDRAs on kidney function and adverse events. MEDLINE, EMBASE, the Cochrane Controlled Trials Register were searched for RCTs that evaluate vitamin D receptor activators (alfacalcidol, calcitriol, doxercalciferol, falecalcitriol, maxacalcitol and paricalcitol) up to March 2015. We included 31 studies, all of which were performed between 1976 and 2015, which enrolled 2621 patients. Patients receiving VDRAs had lower eGFR (weighted mean difference WMD -1.29 mL/min /1.73 m2, 95% CI -2.42 to -0.17) and elevated serum creatinine (WMD 7.03 μmol/L, 95% CI 0.61 to 13.46) in sensitivity analysis excluding studies with dropout rate more than 30%. Subgroup analysis of the 5 studies that not use SCr-based measures did not indicated lower GFR in the VDRAs group(WMD -0.97 mL/min/1.73 m2, 95% CI -4.85 to 2.92). Compared with control groups, there was no difference in all-cause mortality (relative risk RR 1.41, 95% CI 0.58 to 3.80), cardiovascular disease (RR 0.84, 95% CI 0.42 to 1.71), and severe adverse events (RR 1.15, 95% CI 0.75 to 1.77) for the VDRAs groups. Episodes of hypercalcemia (RR 3.29, 95% CI 2.02 to 5.38) were more common in the VDRAs group than in the control group. Administration of VDRAs increased serum creatinine levels. Subgroup analysis of studies that did not use SCr-based measures did not indicate a lower GFR in the VDRA group. Future studies with non-SCr-based measures are needed to assess whether the mild elevations of serum creatinine are of clinical significance.

PMID 26812502
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