更新于：2024-11-01

F11R

更新于：2024-11-01

基本信息

别名

CD321、F11 receptor、F11R

+ [10]

简介

Seems to play a role in epithelial tight junction formation. Appears early in primordial forms of cell junctions and recruits PARD3 (PubMed:11489913). The association of the PARD6-PARD3 complex may prevent the interaction of PARD3 with JAM1, thereby preventing tight junction assembly (By similarity). Plays a role in regulating monocyte transmigration involved in integrity of epithelial barrier (By similarity). Ligand for integrin alpha-L/beta-2 involved in memory T-cell and neutrophil transmigration (PubMed:11812992). Involved in platelet activation (PubMed:10753840). (Microbial infection) Acts as a receptor for Mammalian reovirus sigma-1. (Microbial infection) Acts as a receptor for Human Rotavirus strain Wa.

关联

项与 F11R 相关的药物

JAM-AOE@NV

靶点

F11R

作用机制

F11R modulators

在研机构

同济大学

原研机构

同济大学

在研适应症

雄激素脱发

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

F11R-specific antagonist peptide 4D

靶点

F11R

作用机制

F11R inhibitors

在研机构

State University of New York at Downstate Medical Center

原研机构-

在研适应症

增生

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

F11R program (Provid Pharma)

靶点

F11R

作用机制

F11R inhibitors

在研机构

Provid Pharmaceuticals, Inc.

原研机构

Provid Pharmaceuticals, Inc.

在研适应症

动脉粥样硬化

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 F11R 相关的临床结果

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100 项与 F11R 相关的转化医学

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0 项与 F11R 相关的专利（医药）

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863

项与 F11R 相关的文献（医药）

2025-03-01·Combinatorial Chemistry & High Throughput Screening

Electroacupuncture can Modify Stress, Low-Grade Inflammation in the Duodenum, and Damage to the Intestinal Barrier in Rats with Functional Dyspepsia through the CRF Signaling Pathway

Article

作者: Qi, Chenxi ; Liu, Tong ; Wang, Haili ; Li, Ailin ; Liang, Xurong ; Chen, Lili ; Tan, Ruirui ; Wang, Zhaohui ; Liu, Jiayi

Background:In the domain of functional gastrointestinal disorders, Functional Dyspepsia (FD) stands out due to its widespread occurrence internationally. Historically, electroacupuncture (EA) has been employed as a therapeutic modality for FD, demonstrating notable clinical efficacy.Objectives:This research aimed to delve into the impact of EA on stress responses, minor duodenal inflammatory processes, and the integrity of the intestinal barrier within FD-affected rodent models while also elucidating the underlying mechanisms.Methods:Thirty-six male Wistar rats were evenly distributed into three cohorts: a normal, a modeled FD, and an EA treatment group. The FD condition in the rats, barring those in the normal, was induced through a series of multifactorial procedures. For the EA cohort, the rats received electroacupuncture at the acupoints RN12 (Zhongwan) and ST36 (Zusanli) for 20 minutes daily over a span of one week. The gastric residue rate (GRR), intestinal propulsion rate (IPR), and changes in emotional state were measured in each group of rats. Additionally, serum levels of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and corticosterone (CORT) were detected, and the duodenal inflammatory condition and intestinal mucosal barrier status were observed through staining and fluorescence. The expression levels of Claudin-1, Junctional Adhesion Molecule 1 (JAM-1), Corticotropin-Releasing Factor (CRF), and Corticotropin-Releasing Factor Receptor 1 (CRF-R1) were also detected.Results:The study demonstrated that EA had a positive effect on body weight and food intake, GRR, and IPR in FD rats. Additionally, the EA group showed a decrease in serum levels of CRH, ACTH, and CORT, as well as a decrease in the number of duodenal mast cells and tryptase content. Furthermore, the expression of tight junction proteins Claudin-1 and JAM-1 was increased in the EA group compared to the model group. EA also reduced the levels of CRF and CRF-R1 in the hypothalamus and duodenum.Conclusion:EA has been shown to improve the stress state of FD rats, inhibit the activation of mast cells in the duodenum, and reduce low-grade inflammatory response and damage to the intestinal mucosal barrier. It is believed that EA achieves these effects by modulating the expression of CRF and its receptors in the brain-gut interaction pathway through the CRF signaling pathway. This provides a new approach to treating FD.

2024-10-01·International Journal of Biological Macromolecules

Exploring the anti-inflammatory effects of postbiotic proteins from Lactobacillus delbrueckii CIDCA 133 on inflammatory bowel disease model

Article

作者: de Jesus, Luís Cláudio Lima ; Jan, Gwénaël ; Barroso, Fernanda Alvarenga Lima ; Jardin, Julien ; Campos, Gabriela Munis ; Ferreira, Enio ; Vital, Kátia Duarte ; Viegas, Rhayane Cristina Dos Santos ; Américo, Monique Ferrary ; Laguna, Juliana Guimarães ; Carvalho, Rodrigo Dias de Oliveira ; Freitas, Andria Dos Santos ; Martins, Flaviano Santos ; Gomes, Gabriel Camargos ; Miranda, Ana Paula Gomes Dos Santos ; Fernandes, Simone Odília Antunes ; Azevedo, Vasco

Lactobacillus delbrueckii CIDCA 133 is a promising health-promoting bacterium shown to alleviate intestinal inflammation. However, the specific bacterial components responsible for these effects remain largely unknown. Here, we demonstrated that consuming extractable proteins from the CIDCA 133 strain effectively relieved acute ulcerative colitis in mice. This postbiotic protein fraction reduced the disease activity index and prevented colon shortening in mice. Furthermore, histological analysis revealed colitis prevention with reduced inflammatory cell infiltration into the colon mucosa. Postbiotic consumption also induced an immunomodulatory profile in colitic mice, as evidenced by both mRNA transcript levels (Tlr2, Nfkb1, Nlpr3, Tnf, and Il6) and cytokines concentration (IL1β, TGFβ, and IL10). Additionally, it enhanced the levels of secretory IgA, upregulated the transcript levels of tight junction proteins (Hp and F11r), and improved paracellular intestinal permeability. More interestingly, the consumption of postbiotic proteins modulated the gut microbiota (Bacteroides, Arkkemansia, Dorea, and Oscillospira). Pearson correlation analysis indicated that IL10 and IL1β levels were positively associated with Bacteroides and Arkkemansia_Lactobacillus abundance. Our study reveals that CIDCA 133-derived proteins possess anti-inflammatory properties in colonic inflammation.

2024-09-06·Journal of Proteome Research

Plasma Olink Proteomics Reveals Novel Biomarkers for Prediction and Diagnosis in Dilated Cardiomyopathy with Heart Failure

Article

作者: Xu, Shuai ; Zhang, Ge ; Wang, Xiangyu ; Tan, Xin ; Zeng, Yiyao ; Zhou, Yafeng ; Fan, Huimin ; Jiang, Hezi ; Jiang, Yufeng ; Song, Yahui

In this study, we utilized the Olink Cardiovascular III panel to compare the expression levels of 92 cardiovascular-related proteins between patients with dilated cardiomyopathy combined with heart failure (DCM-HF) (n = 20) and healthy normal people (Normal) (n = 18). The top five most significant proteins, including SPP1, IGFBP7, F11R, CHI3L1, and Plaur, were selected by Olink proteomics. These proteins were further validated using ELISA in plasma samples collected from an additional cohort. ELISA validation confirmed significant increases in SPP1, IGFBP7, F11R, CHI3L1, and Plaur in DCM-HF patients compared to healthy controls. GO and KEGG analysis indicated that NT-pro BNP, SPP1, IGFBP7, F11R, CHI3L1, Plaur, BLM hydrolase, CSTB, Gal-4, CCL15, CDH5, SR-PSOX, and CCL2 were associated with DCM-HF. Correlation analysis revealed that these 13 differentially expressed proteins have strong correlations with clinical indicators such as LVEF and NT-pro BNP, etc. Additionally, in the GEO-DCM data sets, the combined diagnostic value of these five core proteins AUC values of 0.959, 0.773, and 0.803, respectively indicating the predictive value of the five core proteins for DCM-HF. Our findings suggest that these proteins may be useful biomarkers for the diagnosis and prediction of DCM-HF, and further research is prompted to explore their potential as therapeutic targets.

项与 F11R 相关的新闻（医药）

2024-08-16

·微信

皮科文献堂｜张建中教授团队发现：本维莫德可抑制IL-4/IL-13诱导的紧密连接损伤，从而改善特应性皮炎

要点速览 1 生物信息学分析和免疫组化染色显示，特应性皮炎（AD）皮损中CLDN1、CLDN4和OCLN的表达显著下调。 2 体外实验表明，IL-4和IL-13通过Jak/STAT6信号通路下调人永生化角质细胞（HaCaT）和正常人表皮角质形成细胞（NHEKs）中的CLDN1、CLDN4和OCLN表达，并增加细胞旁葡聚糖的通透性。 3 本维莫德通过激活芳基烃受体/芳烃受体核转位蛋白（AHR/ARNT）通路上调CLDN4和OCLN的表达，并诱导NRF2核转位减少角质形成细胞（KC）中的活性氧（ROS），从而抑制IL-4/IL-13诱导的CLDN1下调和STAT6磷酸化。研究背景 AD是一种慢性炎症性皮肤病，病因涉及遗传易感性、皮肤屏障损伤和免疫失调。AD病变的特征包括表皮海绵状病变（细胞间隙增大）和T细胞浸润，特别是T辅助细胞2（Th2），Th1、Th17和Th22细胞也有参与。紧密连接（TJ）封闭细胞间隙，是维持皮肤屏障功能稳定的重要结构。TJ蛋白包括claudins（CLDNs）、occludin（OCLN）、JAM-A、tricellulin、zonula occludens（ZO）和angulins等。既往研究发现，在AD中，这些TJ蛋白的表达往往下调，导致皮肤屏障功能受损，进而促进AD的发展和炎症反应的加剧。 AHR是一种细胞内转录因子，近年来其在AD发病机制和治疗中的作用引起了广泛关注。既往研究表明，AHR参与了TJ的调控。在AD病变中，AHR蛋白的表达增加。也有报道称，IL-4可以在信号转导子和转录激活子6 (STAT6) 依赖的方式下诱导和激活B细胞中的AHR。我国自主研发的创新药物——本维莫德，已被证明对银屑病和AD有效。作为一种AHR激动剂，本维莫德可促进KC分化，并通过其内在特性和部分诱导NRF2通路基因来降低ROS水平，显示出抗氧化活性。北京大学人民医院张建中教授团队进一步分析了Th2细胞因子（IL-4/IL-13）和本维莫德对TJ调控的影响，为AD的治疗提供新的策略。该研究成果于2024年3月表于《Journal of Investigative Dermatology》杂志，（IF=5.7）[1]。研究结果 1 在AD皮损中，TJ蛋白的表达水平普遍下降通过生物信息学分析，基于多个基因表达数据集（GSE130588、GSE133477、GSE32924和GSE133385）发现：在AD皮损中，CLDN1和CLDN4的mRNA水平显著低于非病变皮肤，而OCLN的mRNA水平在AD皮损和非皮损中均比正常皮肤显著降低，但在皮损和非皮损之间无显著差异（图1a,b,c）。免疫组化染色进一步证实，AD皮损中的CLDN1蛋白表达显著低于正常皮肤，而CLDN4和OCLN的蛋白表达虽有下降，但差异不显著（图1d）。图1：生物信息学分析及免疫组化染色评估AD皮损中CLDN1、CLDN4和OCLN的表达水平；注：*P < .05, **P < .01, ***P < .001, ****P < .0001 2 IL-4、IL-13和IFN-γ能够单独下调TJ蛋白的表达使用不同浓度的细胞因子（IL-4、IL-13、TNF-α、IFN-γ和IL-17A）处理HaCaT和NHEKs，结果显示，IL-4、IL-13和IFN-γ显著下调了HaCaT中TJ蛋白（CLDN1、CLDN4和OCLN）的mRNA和蛋白水平，而TNF-α和IL-17A则没有显著影响（图2a,b,c），且IL-4/IL-13之间没有协同效应。在NHEKs中，IL-4/IL-13处理显著降低了CLDN4和OCLN的蛋白水平，但对CLDN1的蛋白水平影响不显著（图2d,e）。图2：IL-4/IL-13对HaCaT及NHEKs中TJ蛋白表达的影响；注：*P < .05, **P < .01, ***P < .001, ****P < .0001 3 IL-4/IL-13和IFN-γ诱导的HaCaT中TJ蛋白表达下调是通过Jak/STAT6信号通路介导的使用Jak1/2抑制剂芦可替尼、STAT6抑制剂AS1517499和STAT1抑制剂氟达拉滨预处理HaCaT。结果显示，芦可替尼剂量依赖性地抑制了IL-4/IL-13和IFN-γ诱导对TJ蛋白（CLDN1、CLDN4和OCLN）mRNA表达的影响（图3a），而STAT6和STAT1抑制剂也有效抑制了以上细胞因子诱导的TJ蛋白下调（图3b）。此外，单独使用IL-4、IL-13或IFN-γ处理KCs会增加细胞旁葡聚糖通量，而同时使用IL-4/IL-13处理则导致更显著的葡聚糖通量增加。用1 mM 芦可替尼预处理HaCaT，可以有效抑制由IL-4/IL-13或IFN-γ诱导增加的葡聚糖通量（图3c）。图3：Jak/STAT通路参与IL-4/IL-13/IFN-γ诱导的HaCa中的TJ蛋白下调；注：*P < .05, **P < .01, ***P < .001, ****P < .0001 4 AHR通路和ROS在IL-4/IL-13诱导的TJ蛋白表达下调中起重要作用 IL-4/IL-13能够上调HaCaT和NHEKs中的AHR（图8a），使用Jak抑制剂芦可替尼、STAT6抑制剂AS1517499和ROS抑制剂二苯乙烯碘化物预处理后可以消除这种上调效应。IL-4/IL-13对典型的AHR通路产物CYP1A1或AHR抑制因子的表达没有影响（图4b）。沉默AHR mRNA的表达可以恢复IL-4/IL-13诱导下调的HaCaT中CLDN1的表达并减少CLDN4和OCLN的表达（图4c），同时增加了磷酸化的STAT6（图4d）。ROS抑制剂二苯乙烯碘化物抑制了IL-4/IL-13诱导的CLDN1下调，但不影响CLDN4或OCLN（图4e）；同时抑制了IL-4/IL-13诱导的磷酸化的STAT6及AHR上调（图4f和g）。图4：AHR通路和ROS参与IL-4/IL-13诱导CLDN1、CLDN4和OCLN表达下调；注：*P < .05, **P < .01, ***P < .001, ****P < .0001 5 本维莫德通过激活AHR/ARNT通路来上调CLDN4和OCLN表达，并阻断IL-4/IL-13或IFN-γ诱导的细胞旁葡聚糖通量增加本维莫德依赖性地上调HaCaT和NHEKs中的CLDN4和OCLN表达，但不影响CLDN1的表达（图5a）。500 nM的本维莫德抑制了由IL-4/IL-13或IFN-γ诱导的跨细胞葡聚糖通量增加（图5b），且不影响细胞增殖（图5c）。本维莫德促进了AHR的核转位（图5d）并上调了CYP1A1和CYP1B1的表达（图5e），而敲除AHR或AHR核转位因子，或用AHR拮抗剂CH-223191预处理，可阻断本维莫德对HaCaT和NHEKs中CLDN4和OCLN表达的影响，同时，本维莫德处理后AHR蛋白水平也有所下降，但AHR mRNA的表达没有明显改变(图5f、g）。图5：本维莫德通过AHR/ARNT通路上调CLDN4和OCLN的表达，并阻断IL-4/IL-13e或IFN基因诱导的细胞旁葡聚糖通量；注：*P < .05, **P < .01, ***P < .001, ****P < .0001 6 本维莫德可抑制IL-4/IL-13诱导的STAT6磷酸化、TJ蛋白表达下调本维莫德促进NHEKs中NRF2的核转位（图6a），并上调NQO1的表达；并能抑制IL-4/IL-13诱导的NHEKs中ROS的产生（图6b）和HaCaT中STAT6的磷酸化（图6c）。本维莫德还抑制了IL-4/IL-13诱导的HaCaT和NHEKs中TJ蛋白表达下调（图6d,e）。另外，本维莫德对IFN-γ诱导的STAT1激活或CLDN1下调没有影响，可恢复CLDN4和OCLN的表达（图6f）。图6：本维莫德抑制IL-4/IL-13诱导的STAT6磷酸化、TJ蛋白表达下调；注：*P < .05, **P < .01, ***P < .001, ****P < .0001 研究结论该研究证实，IL-4/IL-13通过Jak/STAT6信号通路下调TJ蛋白（CLDN1、CLDN4和OCLN）的表达，从而导致KCs中TJ功能损害，促进AD发展。而本维莫德可以激活AHR/ARNT通路，上调CLDN4和OCLN表达，并诱导NRF2核转位减少ROS产生，从而抑制IL-4/IL-13引起的TJ损伤和STAT6磷酸化（图6g）。研究结果显示，本维莫德在保护表皮屏障功能中有潜在作用，为其用于AD治疗提供了新的理论依据，并为开发AD治疗药物提供了重要方向。更多精彩参考文献： [1]Wang X, Mao D, Jia J, Zhang J. Benvitimod Inhibits IL-4- and IL-13-Induced Tight Junction Impairment by Activating AHR/ARNT Pathway and Inhibiting STAT6 Phosphorylation in Human Keratinocytes. J Invest Dermatol. 2024 Mar;144(3):509-519.e7. doi: 10.1016/j.jid.2023.07.027. Epub 2023 Sep 20. PMID: 37734479. 免责声明本微信文章中的信息仅供向医疗卫生专业人士提供科学信息，不可直接作为决策内容，中昊药业不对任何主体因使用本文内容而导致的任何损失承担责任。以上内容如涉版权请联系删除。

AHA会议信使RNA临床结果

2024-03-12

·生物探索

Bioact Mater | 同济大学江华/李宇飞团队通过研究仿生工程ADSC水凝胶治疗脱发

引言2024年3月1日，同济大学江华、李宇飞团队在Bioactive Materials （IF 18.9）发表题为“Bioinspired engineering ADSC nanovesicles thermosensitive hydrogel enhance autophagy of dermal papilla cells for androgenetic alopecia treatment”的研究论文，这是一篇关于治疗雄激素性脱发的研究论文。该研究通过仿生工程的方法，利用脂肪干细胞来源的纳米囊泡和热敏水凝胶，增强了皮肤乳头细胞的自噬作用，从而促进了脱发患者的头发再生。雄激素性脱发是一种常见的非瘢痕性脱发，但目前缺乏有效的治疗方法。干细胞外泌体具有与干细胞相似的修复效果，但成本高、产量低等问题限制了其应用。然而，通过机械挤压获得的细胞源性纳米囊泡具有类似外泌体的优势，能够高效地封装大量的治疗蛋白。研究观察到一种名为JAM-A的粘附蛋白可以显著增加皮肤乳头细胞的粘附性和韧性，从而形成对二氢睾酮和巨噬细胞损伤的快速修复结构，促进脱发患者的头发再生。为了解决JAM-A外泌体的半衰期短的限制，研究人员通过改造脂肪干细胞，使其过表达JAM-A，从而产生了工程化的JAM-A过表达纳米囊泡（JAM-AOE@NV）。将JAM-AOE@NV纳入热敏水凝胶基质（JAM-AOE@NV Gel）中，有效地解决了JAM-AOE@NV半衰期短的问题，并实现了JAM-AOE@NV的持续释放。对JAM-AOE@NV Gel的理化特性进行了分析，并评估了其在体内和体外促进头发再生的疗效。模式图（Credit: Bioactive Materials）这项研究为治疗雄激素性脱发提供了一种新的治疗方法。通过利用纳米囊泡和热敏水凝胶的特性，研究人员成功地增强了皮肤乳头细胞的自噬作用，促进了脱发患者的头发再生。然而，这项研究还需要进一步的实验和临床验证，以确保其安全性和有效性。总的来说，这项研究为治疗雄激素性脱发提供了一种新的治疗策略。通过生物启发工程的方法，利用纳米囊泡和热敏水凝胶，增强了皮肤乳头细胞的自噬作用，从而促进了脱发患者的头发再生。这项研究为进一步的研究和临床应用提供了理论基础，为脱发患者提供了新的治疗选择。原文链接https://doi.org/10.1016/j.bioactmat.2024.02.023责编|探索君排版|探索君文章来源|“iNature”End往期精选围观一文读透细胞死亡(Cell Death) | 24年Cell重磅综述（长文收藏版）热文Nature | 破除传统：为何我们需要重新思考肿瘤的命名方式热文Nature | 2024年值得关注的七项技术热文Nature | 自身免疫性疾病能被治愈吗？科学家们终于看到了希望热文CRISPR技术进化史 | 24年Cell综述

临床结果临床研究

2022-12-22

·PRNewswire

REDUVO™ Marketing Approval on the Right Path

Second Clarifax received from Health Canada. MONTREAL, Dec. 22, 2022 /PRNewswire/ - Tetra Bio-Pharma Inc. ("Tetra" or the "Company") (TSX: TBP) (OTCQB: TBPMF) (FRA: JAM1) a leader in cannabinoid-derived drug discovery and development is providing its shareholders with another regulatory update on the REDUVO™ New Drug Submission (NDS). The last update was provided on November 18, 2022. On December 21, 2022, the Company received a second Clarification Request (Clarifax) from Health Canada regarding the product's Risk Management Plan, which is not atypical for a controlled substance drug. The Company will be submitting the response to Health Canada within the allowed timeframe. The Company cannot comment on Health Canada's response timelines. Questions/feedback from Health Canada are received as the review of the dossier progresses through different review streams. About REDUVO™ REDUVO™ is a soft gel capsule used to treat chemotherapy-induced nausea and vomiting (CINV). It is also used to treat weight loss and severe nausea in people living with HIV infection. The active pharmaceutical ingredient in REDUVO™ is dronabinol, also known as THC, a synthetic form of the active natural substance in cannabis. REDUVO™ 5-year cumulative gross sales expected to reach $121M. About Tetra Bio-Pharma Tetra Bio-Pharma (TSX: TBP) (OTCQB: TBPMF) (FRA:JAM1) is a leader in cannabinoid-derived drug discovery and development with a FDA and a Health Canada cleared clinical program aimed at bringing novel prescription drugs and treatments to patients and their healthcare providers. Their evidence-based scientific approach has enabled them to develop a pipeline of cannabinoid-based drug products for a range of medical conditions, including pain, inflammation, and oncology. With patients at the core of what they do, Tetra Bio-Pharma is focused on providing rigorous scientific validation and safety data required for inclusion into the existing biopharma industry by regulators, physicians and insurance companies. Neither the TSX Exchange nor its Regulation Services Provider (as that term is defined in the policies of the TSX Exchange) accepts responsibility for the adequacy or accuracy of this release. Forward-looking statements Some statements in this release may contain forward-looking information. All statements, other than of historical fact, that address activities, events or developments that the Company believes, expects or anticipates will or may occur in the future (including, without limitation, statements regarding potential acquisitions and financings) are forward-looking statements. Forward-looking statements are generally identifiable by use of the words "may", "will", "should", "continue", "expect", "anticipate", "estimate", "believe", "intend", "plan" or "project" or the negative of these words or other variations on these words or comparable terminology. Forward-looking statements are subject to a number of risks and uncertainties, many of which are beyond the Company's ability to control or predict, that may cause the actual results of the Company to differ materially from those discussed in the forward-looking statements. Factors that could cause actual results or events to differ materially from current expectations include, among other things, without limitation, the inability of the Company to obtain sufficient financing to execute the Company's business plan; competition; regulation and anticipated and unanticipated costs and delays, the success of the Company's research and development strategies, including the success of this product or any other product, the applicability of the discoveries made therein, the successful and timely completion and uncertainties related to the regulatory process, the timing of clinical trials, the timing and outcomes of regulatory or intellectual property decisions and other risks disclosed in the Company's public disclosure record on file with the relevant securities regulatory authorities. Although the Company has attempted to identify important factors that could cause actual results or events to differ materially from those described in forward-looking statements, there may be other factors that cause results or events not to be as anticipated, estimated or intended. Readers should not place undue reliance on forward-looking statements. The forward-looking statements included in this news release are made as of the date of this news release and the Company does not undertake an obligation to publicly update such forward-looking statements to reflect new information, subsequent events or otherwise unless required by applicable securities legislation. SOURCE Tetra Bio-Pharma Inc.

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