Edifoligide sodium(Edifoligide sodium) - 药物靶点：E2F1_专利_临床

概要

基本信息

药物类型

TF Decoy

别名

E2F decoy ODN、E2F duplex decoy、E2F transcription factor decoy

+ [7]

靶点

E2F1

作用机制

E2F1抑制剂(转录因子E2F1抑制剂)

治疗领域

心血管疾病其他疾病泌尿生殖系统疾病

在研适应症-

非在研适应症

动脉闭塞性疾病冠心病血管移植物阻塞+ [4]

原研机构

Anesiva, Inc.

在研机构-

非在研机构

Anesiva, Inc.

最高研发阶段终止临床3期

首次获批日期-

最高研发阶段(中国)-

特殊审评-

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结构

使用我们的RNA技术数据为新药研发加速。

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序列信息

Sequence Code 29359050

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Sequence Code 29883143

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关联

3

项与 Edifoligide sodium 相关的临床试验

NCT00086164 / Terminated临床1/2期

A Phase 1/2, Multi-Center, Randomized, Double-Blind, Placebo-Controlled, Pilot Trial to Assess the Effect of Treatment of the Recipient Vein of a Polytetrafluoroethylene (PTFE) Vascular Access Graft With Two Concentrations of E2F Decoy as Compared to Placebo on Neointimal Hyperplasia and the Preservation of Graft Function in Patients With Chronic Renal Failure Requiring Hemodialysis

The purpose of this study is to determine the effect of recipient vein pretreatment of edifoligide (E2F Decoy), compared to placebo, on graft/recipient vein stenosis in polytetrafluoroethylene (PTFE) vascular access grafts placed for hemodialysis at 6 months after enrollment.

开始日期2004-05-01

申办/合作机构

Anesiva, Inc.

NCT00042081 / Completed临床3期

A Phase III, Multi-Center Randomized, Double-Blind, Placebo-Controlled Trial of the Ex Vivo Treatment With CGT003 of Coronary Vein Grafts in Patients Undergoing Coronary Artery Bypass Graft Procedures

The purpose of this study is to determine the efficacy of graft pretreatment with CGT003 (E2F Duplex Decoy), as compared to placebo, on the incidence of patients experiencing vein graft failure after coronary artery bypass surgery.

开始日期2002-07-01

申办/合作机构

Anesiva, Inc.

NCT00041925 / Completed临床2/3期

A Phase III, Multi-Center Randomized, Double-Blind, Placebo-Controlled Trial of the Ex Vivo Treatment With CGT003 of Peripheral Vein Grafts in Patients Undergoing Peripheral Arterial Bypass Graft Procedures

The purpose of this study is to determine the efficacy of graft pretreatment with the E2F decoy, CGT003, as compared to placebo, on the occurrence of graft failure among patients who receive autogenous vein grafts to treat chronic critical limb ischemia; on the occurrence of clinically significant graft stenosis (more than or equal to 70%); and on the incidence of critical limb ischemia (e.g., gangrene, non-healing ischemic ulcers or ischemic rest pain).

开始日期2001-11-01

申办/合作机构

Anesiva, Inc.

100 项与 Edifoligide sodium 相关的临床结果

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100 项与 Edifoligide sodium 相关的转化医学

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100 项与 Edifoligide sodium 相关的专利（医药）

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70

项与 Edifoligide sodium 相关的文献（医药）

2024-01-01·Oncology Research

Combinational therapy with Myc decoy oligodeoxynucleotides encapsulated in nanocarrier and X-irradiation on breast cancer cells

Article

作者: Sharafi, Ali ; Gharbavi, Mahmoud ; Parvinzad Leilan, Milad ; Johari, Behrooz ; Rezaeejam, Hamed ; Mortazavi, Yousef

The Myc gene is the essential oncogene in triple-negative breast cancer (TNBC). This study investigates the synergistic effects of combining Myc decoy oligodeoxynucleotides-encapsulated niosomes-selenium hybrid nanocarriers with X-irradiation exposure on the MDA-MB-468 cell line. Decoy and scramble ODNs for Myc transcription factor were designed and synthesized based on promoter sequences of the Bcl2 gene. The nanocarriers were synthesized by loading Myc ODNs and selenium into chitosan (Chi-Se-DEC), which was then encapsulated in niosome-nanocarriers (NISM@Chi-Se-DEC). FT-IR, DLS, FESEM, and hemolysis tests were applied to confirm its characterization and physicochemical properties. Moreover, cellular uptake, cellular toxicity, apoptosis, cell cycle, and scratch repair assays were performed to evaluate its anticancer effects on cancer cells. All anticancer assessments were repeated under X-ray irradiation conditions (fractionated 2Gy). Physicochemical characteristics of niosomes containing SeNPs and ODNs showed that it is synthesized appropriately. It revealed that the anticancer effect of NISM@Chi-Se-DEC can be significantly improved in combination with X-ray irradiation treatment. It can be concluded that NISM@Chi-Se-DEC nanocarriers have the potential as a therapeutic agent for cancer treatment, particularly in combination with radiation therapy and in-vivo experiments are necessary to confirm the efficacy of this nano-drug.

2022-11-02·Cancer Immunology Research

Secreted Fas Decoys Enhance the Antitumor Activity of Engineered and Bystander T Cells in Fas Ligand–Expressing Solid Tumors

Article

作者: Bajgain, Pradip ; Balasubramanian, Kishore ; Vera, Juan ; Heslop, Helen E. ; Fleckenstein, Lindsey ; Torres Chavez, Alejandro G. ; Leen, Ann M. ; Lulla, Premal

AbstractT-cell immunotherapy has demonstrated remarkable clinical outcomes in certain hematologic malignancies. However, efficacy in solid tumors has been suboptimal, partially due to the hostile tumor microenvironment composed of immune-inhibitory molecules. One such suppressive agent abundantly expressed in solid tumors is Fas ligand (FasL), which can trigger apoptosis of Fas-expressing effector cells such as T cells and natural killer (NK) cells. To alleviate this FasL-induced suppression of tumor-specific immune cells in solid tumors, we describe here the development of a Fas decoy that is secreted by engineered cells upon activation and sequesters the ligand, preventing it from engaging with Fas on the surface of effector cells. We further improved the immune-stimulatory effects of this approach by creating a Fas decoy and IL15 cytokine fusion protein, which enhanced the persistence and antitumor activity of decoy-engineered as well as bystander chimeric-antigen receptor (CAR) T cells in xenograft models of pancreatic cancer. Our data indicate that secreted Fas decoys can augment the efficacy of both adoptively transferred and endogenous tumor-specific effector cells in FasL-expressing solid tumors.

2021-01-01·Redox Biology1区 · 生物学

Activation of the mechanosensitive Ca2+ channel TRPV4 induces endothelial barrier permeability via the disruption of mitochondrial bioenergetics

1区 · 生物学

ArticleOA

作者: Song, Shanshan ; Yuan, Jason X-J ; Lu, Qing ; Wang, Hui ; Zemskov, Evgeny A ; Kangath, Archana ; Black, Stephen M ; Wu, Xiaomin ; Cabanillas, Gabriela Zubiate ; Tang, Haiyang ; Garcia-Flores, Alejandro ; Wang, Ting ; Yegambaram, Manivannan ; Sun, Xutong ; Fineman, Jeffrey R

Mechanical ventilation is a life-saving intervention in critically ill patients with respiratory failure due to acute respiratory distress syndrome (ARDS), a refractory lung disease with an unacceptable high mortality rate. Paradoxically, mechanical ventilation also creates excessive mechanical stress that directly augments lung injury, a syndrome known as ventilator-induced lung injury (VILI). The specific mechanisms involved in VILI-induced pulmonary capillary leakage, a key pathologic feature of VILI are still far from resolved. The mechanoreceptor, transient receptor potential cation channel subfamily V member 4, TRPV4 plays a key role in the development of VILI through unresolved mechanism. Endothelial nitric oxide synthase (eNOS) uncoupling plays an important role in sepsis-mediated ARDS so in this study we investigated whether there is a role for eNOS uncoupling in the barrier disruption associated with TRPV4 activation during VILI. Our data indicate that the TRPV4 agonist, 4α-Phorbol 12,13-didecanoate (4αPDD) induces pulmonary arterial endothelial cell (EC) barrier disruption through the disruption of mitochondrial bioenergetics. Mechanistically, this occurs via the mitochondrial redistribution of uncoupled eNOS secondary to a PKC-dependent phosphorylation of eNOS at Threonine 495 (T495). A specific decoy peptide to prevent T495 phosphorylation reduced eNOS uncoupling and mitochondrial redistribution and preserved PAEC barrier function under 4αPDD challenge. Further, our eNOS decoy peptide was able to preserve lung vascular integrity in a mouse model of VILI. Thus, we have revealed a functional link between TRPV4 activation, PKC-dependent eNOS phosphorylation at T495, and EC barrier permeability. Reducing pT495-eNOS could be a new therapeutic approach for the prevention of VILI.

100 项与 Edifoligide sodium 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D03949	-	-	DB06556

研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
冠心病	临床3期	美国	Anesiva, Inc.	2002-07-01
动脉闭塞性疾病	临床3期	加拿大	Anesiva, Inc.	2001-11-01
血管移植物阻塞	临床3期	加拿大	Anesiva, Inc.	2001-11-01
血管移植物阻塞	临床3期	美国	Anesiva, Inc.	2001-11-01
增生	临床3期	美国	Anesiva, Inc.	2001-11-01
增生	临床3期	加拿大	Anesiva, Inc.	2001-11-01
缺血	临床3期	加拿大	Anesiva, Inc.	2001-11-01
缺血	临床3期	美国	Anesiva, Inc.	2001-11-01
外周血管疾病	临床3期	美国	Anesiva, Inc.	2001-11-01
外周血管疾病	临床3期	加拿大	Anesiva, Inc.	2001-11-01

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临床结果

适应症

分期

评价

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT00042081 (PREVENT IV, Pubmed \| Am Heart J)	临床3期	-	-	Edifoligide	(顧鏇網觸齋製淵憲醖膚) = 築鏇獵選夢襯繭醖積選憲衊製壓鹹淵淵觸膚範 (窪繭鏇鏇淵繭鏇鏇醖衊 ) 更多	-	2012-09-01
				Placebo	(顧鏇網觸齋製淵憲醖膚) = 蓋網鏇願觸艱衊築鏇遞憲衊製壓鹹淵淵觸膚範 (窪繭鏇鏇淵繭鏇鏇醖衊 ) 更多
NCT00042081 (Prevent IV, Pubmed \| J Coll Physicians Surg Pak)	临床3期	冠状动脉旁路移植术并发症	3,014	Edifoligide	壓蓋壓齋廠蓋繭積鹽艱(糧鏇範觸壓觸繭鹹遞淵) = 醖積網廠構繭積繭艱餘繭齋窪鑰遞夢齋齋網壓 (獵鑰艱構齋糧製獵願積 ) 更多	不佳	2005-11-16
				Placebo	壓蓋壓齋廠蓋繭積鹽艱(糧鏇範觸壓觸繭鹹遞淵) = 齋顧願選選範壓醖範鹽繭齋窪鑰遞夢齋齋網壓 (獵鑰艱構齋糧製獵願積 ) 更多