预约演示

更新于：2025-05-07

TAFA5

更新于：2025-05-07

基本信息

别名

Chemokine-like protein TAFA-5、FAM19A5、TAFA chemokine like family member 5

+ [2]

简介

Acts as a chemokine-like protein by regulating cell proliferation and migration through activation of G protein-coupled receptors (GPCRs), such as S1PR2 and FPR2 (By similarity). Stimulates chemotactic migration of macrophages mediated by the MAPK3/ERK1 and AKT1 pathway (By similarity). Blocks TNFSF11/RANKL-induced osteoclast formation from macrophages by inhibiting up-regulation of osteoclast fusogenic and differentiation genes (By similarity). Stimulation of macrophage migration and inhibition of osteoclast formation is mediated via GPCR FPR2 (By similarity). Acts as an adipokine by negatively regulating vascular smooth muscle cell (VSMC) proliferation and migration in response to platelet-derived growth factor stimulation via GPCR S1PR2 and G protein GNA12/GNA13-transmitted RHOA signaling (By similarity). Inhibits injury-induced cell proliferation and neointima formation in the femoral arteries (By similarity).

关联

项与 TAFA5 相关的药物

NS-101(Neuracle Science)

靶点

TAFA5

作用机制

TAFA5 modulators

在研机构

Neuracle Science Co., Ltd.

原研机构

Neuracle Science Co., Ltd.

在研适应症

神经性听力损失 [+2]

非在研适应症-

最高研发阶段临床1/2期

首次获批国家/地区-

首次获批日期1800-01-20

NS-300

靶点

TAFA5

作用机制

TAFA5 modulators

在研机构

Neuracle Science Co., Ltd.

原研机构

Neuracle Science Co., Ltd.

在研适应症

感觉障碍

非在研适应症

自闭症 [+3]

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

NS-350

靶点

TAFA5

作用机制

TAFA5 modulators

在研机构

Neuracle Science Co., Ltd.

原研机构

Neuracle Science Co., Ltd.

在研适应症

阿尔茨海默症 [+1]

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

项与 TAFA5 相关的临床试验

NCT06249919

/ Recruiting临床1/2期

A Phase 1b/2a, Double-blinded, Placebo-controlled, Multiple Doses, 2 Step-up Study Evaluating the Safety, Tolerability, PK/PD and Efficacy of Systemic NS101 in Healthy Volunteers and SSNHL Patients

The goal of this 2 step-up, exploratory study is to test safey, tolerability and PK/PD profiles in healthy volunteers and safety, tolerability and efficacy in sudden sensorineural hearing loss patients as an early salvage therapy.
The main questions it aims to answer are:
1. whether is it safe and tolerable when healthy volunteers and sudden sensorineural hearing loss patients take multiple doses of NS101 against FAM19A5
2. whether is it effective in reversing hearing capability in sudden sensorineural hearing loss patients who fails to show sufficient recovery despite of oral standard steroid therapy.
Patients and heathly volunteers will be given NS101 15mg/kg or 30mg/kg systemically less than 3 months per protocol.
This is placebo controlled, double blinded study, which means there will be a group who receives placebo (i.e. fake drug) for study purpose.

开始日期2024-01-19

申办/合作机构

Neuracle Science Co., Ltd.

[+3]

NCT05143463

/ Completed临床1期

A Phase 1, Randomized, Placebo-controlled, Double-blind, Single Ascending Dose Study to Assess the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of Intravenous NS101 Infusion in Healthy Volunteers

Up to 80 healthy adult males, ≥ 18 and ≤ 55 years of age, are planned to be enrolled in the study.
The study will consist of 8 cohorts (Cohorts 1 to 8, 1 cohort per dose level). Each cohort will include 8 subjects (6 subjects receiving a single dose of the study drug NS101 and 2 subjects receiving a single dose of a matching placebo), for a total of 64 subjects planned for evaluation. A total of 21 blood samples will be collected in each cohort for PK analysis and a total of 14 blood samples will be collected in each cohort for PD analysis.

开始日期2021-11-04

申办/合作机构

Neuracle Science Co., Ltd.

100 项与 TAFA5 相关的临床结果

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100 项与 TAFA5 相关的转化医学

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0 项与 TAFA5 相关的专利（医药）

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项与 TAFA5 相关的文献（医药）

2024-12-01·Neural Regeneration Research

Biomarkers for neuromyelitis optica: a visual analysis of emerging research trends

Article

作者: Shi, Shengling ; Li, Chunyan ; Leng, Ying ; Zhang, Siqi ; Li, Xiangjun ; Zhang, Jiandong ; Lu, Yi’an

Neuromyelitis optica is an inflammatory demyelinating disease of the central nervous system that differs from multiple sclerosis. Over the past 20 years, the search for biomarkers for neuromyelitis optica has been ongoing. Here, we used a bibliometric approach to analyze the main research focus in the field of biomarkers for neuromyelitis optica. Research in this area is consistently increasing, with China and the United States leading the way on the number of studies conducted. The Mayo Clinic is a highly reputable institution in the United States, and was identified as the most authoritative institution in this field. Furthermore, Professor Wingerchuk from the Mayo Clinic was the most authoritative expert in this field. Keyword analysis revealed that the terms “neuromyelitis optica” (261 times), “multiple sclerosis” (220 times), “neuromyelitis optica spectrum disorder” (132 times), “aquaporin 4” (99 times), and “optical neuritis” (87 times) were the most frequently used keywords in literature related to this field. Comprehensive analysis of the classical literature showed that the majority of publications provide conclusive research evidence supporting the use of aquaporin-4-IgG and neuromyelitis optica-IgG to effectively diagnose and differentiate neuromyelitis optica from multiple sclerosis. Furthermore, aquaporin-4-IgG has emerged as a highly specific diagnostic biomarker for neuromyelitis optica spectrum disorder. Myelin oligodendrocyte glycoprotein-IgG is a diagnostic biomarker for myelin oligodendrocyte glycoprotein antibody-associated disease. Recent biomarkers for neuromyelitis optica include cerebrospinal fluid immunological biomarkers such as glial fibrillary acidic protein, serum astrocyte damage biomarkers like FAM19A5, serum albumin, and gamma-aminobutyric acid. The latest prospective clinical trials are exploring the potential of these biomarkers. Preliminary results indicate that glial fibrillary acidic protein is emerging as a promising candidate biomarker for neuromyelitis optica spectrum disorder. The ultimate goal of future research is to identify non-invasive biomarkers with high sensitivity, specificity, and safety for the accurate diagnosis of neuromyelitis optica.

2024-12-01·Molecules and Cells

Is FAM19A5 an adipokine? Peripheral FAM19A5 in wild-type, FAM19A5 knockout, and LacZ knockin mice

Article

作者: Kwon, Soon-Gu ; Hwang, Jong-Ik ; Lee, Yoo-Na ; Cho, Eun Bee ; Cho, Eun-Ho ; Reyes-Alcaraz, Arfaxad ; Kwak, Hoyun ; Shahapal, Anu ; Oh, Sitaek ; Lee, Yerim ; Kim, Won Kyum ; Jeong, Yongwoo ; Yong, Hyo Jeong ; Yoo, Sangjin ; Seong, Jae Young ; Lee, Jae Keun ; Ha, Nui ; Lee, Minhyeok ; Lee, Won Suk

FAM19A5 is a novel secretory protein expressed primarily in the brain. However, a recent study reported that FAM19A5 is an adipocyte-derived adipokine that regulates vascular smooth muscle function through sphingosine-1-phosphate receptor 2 (S1PR2). In our study, we investigated FAM19A5 transcript and protein levels in peripheral tissues, including adipose tissues, from wild-type, FAM19A5 knockout, and FAM19A5-LacZ knockin mice. We found that the FAM19A5 transcript levels in the central nervous system were much greater than those in any of the peripheral tissues, including adipose tissues. Furthermore, the FAM19A5 protein levels in adipose and reproductive tissues were below detectable limits for Western blot analysis and enzyme-linked immunosorbent assay (ELISA). Additionally, we found that the FAM19A5 protein did not interact with S1PR2 in terms of G-protein-mediated signal transduction, β-arrestin recruitment, or ligand-mediated internalization. Taken together, our findings revealed basal levels of FAM19A5 transcripts and proteins in peripheral tissues, confirming its primary expression in the central nervous system and lack of significant interaction with S1PR2.

2024-08-31·Experimental Neurobiology

FAM19A5 Deficiency Mitigates the Aβ Plaque Burden and Improves Cognition in Mouse Models of Alzheimer's Disease

Article

作者: Park, Sumi ; Hwang, Jong-Ik ; Lee, Sang-Myeong ; Yoo, Sangjin ; Lee, Minhyeok ; Seong, Jae Young ; Kwak, Hoyun ; Shahapal, Anu

FAM19A5, a novel secretory protein highly expressed in the brain, is potentially associated with the progression of Alzheimer's disease (AD). However, its role in the AD pathogenesis remains unclear. Here, we investigated the potential function of FAM19A5 in the context of AD. We generated APP/PS1 mice with partial FAM19A5 deficiency, termed APP/PS1/FAM19A5^+/LacZ mice. Compared with control APP/PS1 mice, APP/PS1/FAM19A5^+/LacZ mice exhibited significantly lower Aβ plaque density and prolonged the lifespan of the APP/PS1 mice. To further explore the therapeutic potential of targeting FAM19A5, we developed a FAM19A5 antibody. Administration of this antibody to APP/PS1 mice significantly improved their performance in the Y-maze and passive avoidance tests, indicating enhanced cognitive function. This effect was replicated in 5XFAD mice, a model of early-onset AD characterized by rapid Aβ accumulation. Additionally, FAM19A5 antibody treatment in 5XFAD mice led to enhanced exploration of novel objects and increased spontaneous alternation behavior in the novel object recognition and Y-maze tests, respectively, indicating improved cognitive function. These findings suggest that FAM19A5 plays a significant role in AD pathology and that targeting with FAM19A5 antibodies may be a promising therapeutic strategy for AD.