Delving into the Latest Updates on Eldecalcitol with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

1α,25-dihydroxy-2β-(3-hydroxypropoxy)cholecalciferol, Eldecalcitol (JAN/INN)

+ [4]

Target

VDR

Mechanism

VDR agonists(Vitamin D receptor agonists)

Therapeutic Areas

Endocrinology and Metabolic DiseaseSkin and Musculoskeletal Diseases

Active Indication

Osteoporosis

Inactive Indication

Osteoporotic FracturesPrimary osteoporosis

Originator Organization

Chugai Pharmaceutical Co., Ltd.

Active Organization

Chugai Pharmaceutical Co., Ltd.

Inactive Organization

Chugai Pharmaceutical Company Limited Beijing Representative Office

Drug Highest PhaseApproved

First Approval Date

JP (21 Jan 2011),

Osteoporosis

Regulation-

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Structure

Molecular FormulaC30H50O5

InChIKeyFZEXGDDBXLBRTD-AYIMTCTASA-N

CAS Registry104121-92-8

主要目的：以北京斯利安药业有限公司提供的艾地骨化醇软胶囊（规格：0.75μg）为受试制剂，原研Chugai Pharmaceutical Co.,Ltd持证的艾地骨化醇软胶囊（规格：0.75μg，商品名：Edirol®）为参比制剂，在空腹和餐后状态下评价受试制剂同参比制剂的生物等效性。次要目的：观察空腹和餐后状态下受试制剂艾地骨化醇软胶囊和参比制剂艾地骨化醇软胶囊（Edirol®）在健康受试者中的安全性。

[Translation]

Primary objective: To evaluate the bioequivalence of the test preparation with the reference preparation under fasting and postprandial conditions, using the edicalcitol soft capsules (specification: 0.75μg) provided by Beijing Silian Pharmaceutical Co., Ltd. as the test preparation and the edicalcitol soft capsules (specification: 0.75μg, trade name: Edirol®) certified by Chugai Pharmaceutical Co., Ltd. as the reference preparation. Secondary objective: To observe the safety of the test preparation edicalcitol soft capsules and the reference preparation edicalcitol soft capsules (Edirol®) in healthy subjects under fasting and postprandial conditions.

Start Date13 Aug 2024

Sponsor / Collaborator

Beijing Silian Pharmaceutical Co., Ltd.

NCT06537115 / RecruitingPhase 4IIT

Clinical Intervention of Idecalcitol Combined With Whey Protein Powder and Exercise for Sarcopenia：a RCT Trial

This clinical trial is a multicenter, single-blind, prospective, randomized controlled clinical application study. Subjects who met the trial criteria and signed the informed consent form were randomly divided into a control group, an experimental group 1, and an experimental group 2. After enrollment, the control group underwent a comprehensive assessment of their underlying conditions by professional physicians and received routine interventions, including basic nutritional intervention program guidance, progressive resistance exercise intervention program guidance, safety precautions, and symptomatic treatment for different complications, for a total intervention period of 24 weeks. The experimental group 1, in addition to the interventions provided to the control group, received whey protein powder supplementation for 12 weeks. The experimental group 2, on the other hand, received both whey protein powder and eldecalcitol supplementation on top of the interventions given to the control group, also for 12 weeks. The entire intervention period lasted for 24 weeks. Through regular general assessments, blood tests, measurements of muscle mass, muscle strength, and physical function, as well as analyses of negative adverse events, statistical methods were employed to evaluate the safety and efficacy of the comprehensive intervention methods for sarcopenia.

Start Date16 Jun 2024

Sponsor / Collaborator

Zhejiang Provincial Peoples Hospital

NCT06385093 / Not yet recruitingPhase 4IIT

Efficacy and Safety of Eldecalcitol in Preventing Glucocorticoid-induced Bone Loss in Rheumatoid Arthritis Patients (ELEGANT)

The study will be a multi-center, randomized, open label, parallel trial conducted in rheumatoid arthritis patients treated with glucocorticoids. After signing the informed consent, all patients will be screened as per the inclusion and exclusion criteria. Estimated 314 eligible patients will be enrolled. The enrolled patients will be randomly assigned to either Eldecalcitol group or Alfacalcidol group in a 1:1 ratio and followed up for 12 months. On-site follow up visits will be conducted at Month 6 and 12 after enrollment. The study is designed to evaluate the efficacy and safety of Eldecalcitol in preventing glucocorticoid-induced bone loss in rheumatoid arthritis patients.

Start Date01 Jun 2024

Sponsor / Collaborator

Chinese SLE Treatment And Research Group

100 Clinical Results associated with Eldecalcitol

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100 Translational Medicine associated with Eldecalcitol

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100 Patents (Medical) associated with Eldecalcitol

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260

Literatures (Medical) associated with Eldecalcitol

01 Dec 2024·Cellular and Molecular Life Sciences

Eldecalcitol ameliorates diabetic osteoporosis and glucolipid metabolic disorder by promoting Treg cell differentiation through SOCE

Article

Author: Li, Xiaolin ; Ying, Qiaohui ; Li, Minqi ; Jiang, Yujun ; Hasegawa, Tomoka ; Song, Aimei ; Gao, Ruihan ; Liu, Hongrui ; Dai, Yaling

Active vitamin D, known for its role in promoting osteoporosis, has immunomodulatory effects according to the latest evidence. Eldecalcitol (ED-71) is a representative of the third-generation novel active vitamin D analogs, and its specific immunological mechanisms in ameliorating diabetic osteoporosis remain unclear. We herein evaluated the therapeutic effects of ED-71 in the context of type 2 diabetes mellitus (T2DM), delving into its underlying mechanisms. In a T2DM mouse model, ED-71 attenuated bone loss and marrow adiposity. Simultaneously, it rectified imbalanced glucose homeostasis and dyslipidemia, ameliorated pancreatic β-cell damage and hepatic glycolipid metabolism disorder. Subsequently, in mice injected with the Treg cell-depleting agent CD25, we observed that the beneficial effects of ED-71 mentioned earlier were partially contingent on the Treg subsets ratio. Mechanistically, ED-71 promoted the differentiation of CD4⁺ T cells into Treg subsets, facilitating Ca²⁺ influx and the expression of ORAI1 and STIM1, pivotal proteins in store-operated Ca²⁺ entry (SOCE). The SOCE inhibitor, 2-APB, partially attenuated the positive effects of ED-71 observed in the above results. Overall, ED-71 regulates SOCE-mediated Treg cell differentiation, accomplishing the dual purpose of simultaneously ameliorating diabetic osteoporosis and glucolipid metabolic disorders, showcasing its potential in osteoimmunity therapy and interventions for diseases involving SOCE.

08 Nov 2024·JCI Insight

Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease

Article

Author: Sato, Amy Y ; Schaible, Eric ; Bellido, Teresita ; Alliston, Tamara ; Boerma, Marjan ; Willis, Monte S. ; Shutter, Jennifer ; Willis, Monte S ; McAndrews, Kevin ; Cregor, Meloney ; Schurman, Charles A ; Sato, Amy Y. ; Adhikari, Bhawana ; Schurman, Charles A. ; Vyas, Punit

Despite their beneficial actions as immunosuppressants, glucocorticoids (GC) have devastating effects on the musculoskeletal and cardiac systems, as long-term treated patients exhibit high incidence of falls, bone fractures, and cardiovascular events. Herein, we show that GC upregulate simultaneously in bone, skeletal muscle, and the heart the expression of E3 ubiquitin ligases (atrogenes), known to stimulate the proteasomal degradation of proteins. Activation of vitamin D receptor (VDR) signaling with the VDR ligands calcitriol or eldecalcitol prevented GC-induced atrogene upregulation in vivo and ex vivo in bone/muscle organ cultures and preserved tissue structure/mass and function of the 3 tissues in vivo. Direct pharmacologic inhibition of the proteasome with carfilzomib also conferred musculoskeletal protection. Genetic loss of the atrogene MuRF1-mediated protein ubiquitination in ΔRING mice afforded temporary or sustained protection from GC excess in bone or skeletal and heart muscle. We concluded that the atrogene pathway downstream of MuRF1 underlies GC action in bone, muscle, and the heart, and it can be pharmacologically or genetically targeted to confer protection against the damaging actions of GC simultaneously in the 3 tissues.

01 Oct 2024·Journal of Oral Biosciences

ED-71 promotes osseointegration of titanium implants in a rat model of GIOP by alleviating the effects of dexamethasone on bone remodeling in a SIRT1-dependent manner

Article

Author: Li, Minqi ; Li, Chunying ; Ma, Jie ; Song, Ailing ; Duan, Guanglin ; Xue, Pengfei ; Zhai, Runbing

OBJECTIVEGlucocorticoid-induced osteoporosis (GIOP), a common complication of glucocorticoid usage, plays a critical role in the success of dental implant restoration by affecting osseointegration. Eldecalcitol (ED-71) prevents GIOP; however, its role in the osseointegration of implants under GIOP conditions remains elusive.METHODSDexamethasone was used to establish a rat model of GIOP. Subsequently, mini-implant surgery was performed on the femur. GIOP rats were administered ED-71 via gavage to assess its role in the osseointegration of titanium implants under GIOP conditions. MC3T3-E1 and RAW264.7 cells were utilized to explore the molecular mechanism of ED-71 in ameliorating disorder of bone remodeling caused by dexamethasone.RESULTSThe administration of ED-71 promoted the formation of newly formed woven bone and the resolution of inflammation around titanium implants. In vitro experiments indicated that ED-71 ameliorated dexamethasone-induced dysfunction of osteoblasts and osteoclasts by increasing the expression level of sirtuin 1 (SIRT1). Inhibition of SIRT1 by selisistat counteracts the regulatory effects of ED-71 on dexamethasone-induced disorder of bone remodeling. Molecular docking and Western blotting revealed that the neurogenic locus notch homolog protein and nuclear factor kappa B signaling pathways are essential for the effects of ED-71 on dexamethasone-induced disorder of bone remodeling.CONCLUSIONED-71 promoted implant osseointegration in a rat model of GIOP by alleviating the effects of dexamethasone on bone remodeling in a SIRT1-dependent manner.

100 Deals associated with Eldecalcitol

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External Link

KEGG	Wiki	ATC	Drug Bank
D07578	Eldecalcitol	A11C	DB05295

R&D Status

10 top approved records.

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Indication	Country/Location	Organization	Date
Osteoporosis	JP	Chugai Pharmaceutical Co., Ltd.	21 Jan 2011

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ASN2016	Not Applicable	-	-	Eldecalcitol	ssymuynliw(ulzgpjldfa) = dqtqtfurkw wycerpfdyj (pvmiepodyp )	Negative	15 Nov 2016
				Placebo	ssymuynliw(ulzgpjldfa) = bqrwgloced wycerpfdyj (pvmiepodyp )
SP588 (ERA2014)	Not Applicable	-	-	Eldecalcitol	jmsoukjslu(bmjqzifupm) = peolzeozmb weycsajhuj (zkbfcrjbah )	Positive	01 May 2014
				Eldecalcitol + Raloxifen	jmsoukjslu(bmjqzifupm) = lgsqwbutcn weycsajhuj (zkbfcrjbah )
NCT00144456 (Pubmed \| Bone)	Phase 3	Osteoporotic Fractures	1,054	Eldecalcitol 0.75 μg	sconguaxnq(kvfpecwrtd) = rnlicqwufu zwjyvgzaop (vompjkfsho, 0.56 - 0.97)	Positive	01 Oct 2011
				Alfacalcidol 1.0 μg	sconguaxnq(kvfpecwrtd) = yxicwwdetd zwjyvgzaop (vompjkfsho )
ASN2010	Not Applicable	Hypoparathyroidism	-	Eldecalcitol	ptqpnadhyq(jkazaafpxx) = ygvrztxdhe oftbzttffj (wwoinvprfi )	-	16 Nov 2010
				Calcitriol	ptqpnadhyq(jkazaafpxx) = jdbkktfwcq oftbzttffj (wwoinvprfi )