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2

项与 Navigen, Inc. 相关的药物

HTRA-1 mAbs (Navigen)

靶点

Serine protease

作用机制

丝氨酸蛋白酶家族抑制剂

在研机构-

原研机构

Navigen, Inc.初创企业

在研适应症-

非在研适应症

黄斑变性

最高研发阶段无进展

首次获批国家/地区-

首次获批日期-

CPT-31

靶点

gp41

作用机制

gp41抑制剂

在研机构-

原研机构

Navigen, Inc.初创企业

在研适应症-

非在研适应症

HIV感染

最高研发阶段无进展

首次获批国家/地区-

首次获批日期-

1

项与 Navigen, Inc. 相关的临床试验

NCT04672083 / Completed临床1期

A Phase Ia Clinical Study of HIV Entry Inhibitor CPT31: Single Ascending Dose Study of Safety, Tolerability, Immunogenicity, and Pharmacokinetics in Healthy Adults

This first-in-human study will evaluate the safety, tolerability, immunogenicity, and pharmacokinetics of the HIV entry inhibitor CPT31 (cholesterol-PIE12-2-trimer) in healthy adults. This is a randomized, placebo-controlled, double-blind, single ascending dose study.

开始日期2020-11-16

申办/合作机构

Navigen, Inc.初创企业

[+2]

100 项与 Navigen, Inc. 相关的临床结果

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0 项与 Navigen, Inc. 相关的专利（医药）

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8

项与 Navigen, Inc. 相关的文献（医药）

2020-09-08·Proceedings of the National Academy of Sciences1区 · 综合性期刊

Prevention and treatment of SHIVAD8 infection in rhesus macaques by a potent d -peptide HIV entry inhibitor

1区 · 综合性期刊

Article

作者: Smith, Amanda R. ; Donau, Olivia K. ; Kay, Michael S. ; Francis, J. Nicholas ; Jesteadt, Eric ; Seaman, Michael S. ; Welch, Brett D. ; Martin, Malcolm A. ; Sadjadpour, Reza ; Nishimura, Yoshiaki

Significance This paper characterizes a d -peptide HIV entry inhibitor, CPT31, in rhesus macaques. This nonhuman primate animal model provides the most robust evaluation of an in vivo antiviral prior to human trials. As described here, CPT31 is a promising HIV drug candidate because of its high potency and breadth, long half-life, and strong activity in this macaque model (both as a preventative and therapeutic agent). The efficacy data described here complete CPT31’s preclinical studies, with clinical trials scheduled to start this year. These data also help establish d -peptides as an emerging class of therapeutics.

2020-05-11·Translational Vision Science & Technology3区 · 医学

Apigenin and Ethaverine Hydrochloride Enhance Retinal Vascular Barrier In Vitro and In Vivo

3区 · 医学

ArticleOA

作者: Tong, Zongzhong ; Chen, Huan ; Jiang, Weiwei ; Tai, Zhengfu ; Zhu, Weiquan ; Luo, Ling ; Li, Tian

PurposeThis study aims to develop an impedance-based drug screening platform that will help identify drugs that can enhance the vascular barrier function by stabilizing vascular endothelial cell junctions.MethodsChanges in permeability of cultured human retinal microvascular endothelial cells (HRMECs) monolayer were monitored in real-time with the xCELLigence RTCA system. Using this platform, we performed a primary screen of 2100 known drugs and confirmed hits using two additional secondary permeability assays: the transwell permeability assay and the XPerT assay. The cellular and molecular mechanisms of action and in vivo therapeutic efficacy were also assessed.ResultsEleven compounds blocked interleukin 1 beta (IL-1β) induced hyperpermeability in the primary screen. Two of 11 compounds, apigenin and ethaverine hydrochloride, reproducibly blocked multiple cytokines induced hyperpermeability. In addition to HRMEC monolayers, the two compounds stabilized three other types of primary vascular endothelial cell monolayers. Preliminary mechanistic studies suggest that the two compounds stabilize the endothelium by blocking ADP-ribosylation factor 6 (ARF6) activation, which results in enhanced VE-cadherin membrane localization. The two compounds showed in vivo efficacy in an animal model of retinal permeability.ConclusionsWe developed an impedance-based cellular phenotypic drug screening platform that can identify drugs that enhance vascular barrier function. We found apigenin and ethaverine hydrochloride stabilize endothelial cell junctions and enhance the vascular barrier by blocking ARF6 activation and increasing VE-cadherin membrane localization.Translational RelevanceThe drugs identified from the phenotypic screen would have potential therapeutic efficacy in retinal vascular diseases regardless of the underlying mechanisms that promote vascular leak.

2019-01-02·Small GTPases

The small GTPase ARF6 regulates protein trafficking to control cellular function during development and in disease

Article

作者: Winter, Jacob M ; Grossmann, Allie H ; Zhu, Weiquan ; Yoo, Jae Hyuk ; Rich, Bianca ; Odelberg, Shannon J ; Zhao, Helong ; Jenkins, Noah ; Richards, Jackson R ; Li, Dean Y ; Mleynek, Tara M

The activation of the small GTPase ARF6 has been implicated in promoting several pathological processes related to vascular instability and tumor formation, growth, and metastasis. ARF6 also plays a vital role during embryonic development. Recent studies have suggested that ARF6 carries out these disparate functions primarily by controlling protein trafficking within the cell. ARF6 helps direct proteins to intracellular or extracellular locations where they function in normal cellular responses during development and in pathological processes later in life. This transport of proteins is accomplished through a variety of mechanisms, including endocytosis and recycling, microvesicle release, and as yet uncharacterized processes. This Commentary will explore the functions of ARF6, while focusing on the role of this small GTPase in development and postnatal physiology, regulating barrier function and diseases associated with its loss, and tumor formation, growth, and metastasis.

100 项与 Navigen, Inc. 相关的药物交易

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100 项与 Navigen, Inc. 相关的转化医学

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