Lung transplant recipient survival lags other solid organ recipients, with the main early cause of death being primary graft dysfunction (PGD). PGD occurs in up to 1/3 of all recipients, is driven by the body's innate immune response, and has no known medical therapies for treatment or prevention. Investigators have recently shown that Natural Killer (NK) cells, a key innate immune cell, are critical in causing PGD. Importantly, the investigators found that Maraviroc, an FDA-approved drug that works to inhibit these immune cells, prevented lung injury in mouse models of PGD.
The goal of this clinical trial is to learn if Maraviroc works to treat PGD in Lung Transplant patients who are above the age of 18 and have a PGD risk score greater than 50%. The objectives the study hopes to address are:
To address the safety and tolerability of Maraviroc. To test a strategy for PGD enrichment in a lung transplant population. To measure the efficacy and biological efficacy of using Maraviroc. To study the biochemical, physiologic, and molecular effects of the drug on the body.
This will be a double blind study where patients will either get the Maraviroc drug or a placebo. Researchers will then compare the two groups to address the above objectives.
Participants will:
Take drug Maraviroc or a placebo every 12 hours for 3 days post surgery. Follow up will occur during the entire length of stay at UCSF, about 16 days, with a single 12 month follow up once released.

开始日期2025-12-07

申办/合作机构

The University of California, San Francisco

[+1]

NCT06805656

/ Not yet recruiting临床2期IIT

Multi Interventional Approaches to Mitigate HIV Reservoirs Aiming the Sustained HIV Remission Without Use of Antiretrovirals

A modern and urgent challenge in fighting HIV infection is to achieve sustained HIV remission without the use of antiretrovirals. The investigators' preliminary data indicate that the use of combined strategies to mitigate the HIV proviral reservoir size among individuals with suppressive antiretroviral treatment achieved unprecedented results in the reduction of HIV DNA present in these cells and in the reduction of CD4 + and CD8 + T cell activation. Combined interventions include intensified antiretroviral treatment to mitigate residual HIV replication, use of a histone deacetylase inhibitor to interrupt viral latency, use of an anti-proliferative medication to reduce long-lived T cells that harbor HIV and a personalized dendritic cell therapy vaccine to eliminate cells with latent HIV infection or cells present in viral sanctuaries. Due to the good results obtained in the exploratory stage of the project, the investigators propose to expand it by recruiting a larger number of patient to confirm the previously obtained results and to generate new insights related to the mechanisms involved in viral latency, latency disruption and the effects of analytical treatment interruption of antiretrovirals among patients undergoing all above mentioned interventions.

开始日期2025-09-01

申办/合作机构

Universidade Federal De Sao Paulo

[+1]

NCT06974084

/ Not yet recruiting临床2/3期

A Multi-Center Randomized, Double-Blind, Placebo-Controlled Study to Evaluate the Efficacy of Maraviroc and Atorvastatin for the Treatment of Subjects With Long COVID/Post-Acute Sequalae of Covid (PASC)

The IMPACT Long Covid Treatment clinical study (IMPACT-LC) is testing two repurposed and previously approved drugs, Maraviroc and Atorvastatin, for the treatment of non-hospitalized subjects with long COVID/Post-Acute Sequelae of COVID (PASC). The main goals of the clinical study are to determine if this combination drug therapy can improve neurocognitive and physical functions in Long Covid patients, such as fatigue severity, heart rate, blood pressure, digestion, breathing, dizziness, and cognitive function. A secondary goal is to determine if biomarker levels, measured by a diagnostic test, can improve during treatment. To qualify for the trial, a subject must be an adult ≥ 18 and ≤ 65 years of age and meets the WHO-defined post-COVID-19 condition and has one or more new-onset Long Covid symptom that persist ≥ 6 months after the diagnosis of acute COVID-19 infection. A total of 252 participants will take either two daily doses of two existing medications (Maraviroc and Atorvastatin together as separate tablets) or a placebo (pills with no active ingredient) for 16 weeks. Although these medications are not yet approved for Long Covid, they are FDA-approved for use in treating other health conditions.

开始日期2025-09-01

申办/合作机构-

100 项与马拉韦罗相关的临床结果

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100 项与马拉韦罗相关的转化医学

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100 项与马拉韦罗相关的专利（医药）

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项与马拉韦罗相关的文献（医药）

2026-04-01·MICROBIAL PATHOGENESIS

Article

作者: Xiao, Yishu ; Hei, Zhiping ; Tian, Chuchu ; Zhang, Zhijie ; Si, Shengbin ; Ren, Xiang ; Sun, Yuning ; Wei, Yin

Rho-associated kinase 1 (ROCK1) is a host kinase involved in the regulation of cytoskeletal dynamics, vesicle trafficking, and cell cycle control; however, its role in parvoviral infection remains largely unexplored. Building on our previous finding that minute virus of canines (MVC) activates the ROCK1/MLC2 signaling pathway to disrupt tight junction integrity and expose the Occludin coreceptor, we further investigated the role of ROCK1 signaling in MVC entry and replication. We demonstrate that ROCK1 exerts distinct, stage-specific roles during MVC infection. At the early stage of MVC infection, ROCK1 activation triggers the ROCK1/LIMK1/CFL1 pathway and NHE1-mediated intracellular alkalinization, promoting cytoskeletal remodelling and facilitating viral entry. Treatment with a ROCK inhibitor or siRNA-mediated ROCK1 knockdown disrupted cytoskeletal rearrangements, reduced NHE1 expression and CFL1 phosphorylation, and impaired viral internalisation. However, during later stages of infection, selective ROCK1 knockdown enhanced MVC replication and viral protein expression. ROCK1 was found to translocate into the nucleus and colocalize with MVC nonstructural proteins NS1 and NP1. Mechanistically, ROCK1 suppression was associated with altered G1/S regulators, including reduced p53/p21/cyclin D1 and increased cyclin E expression, leading to prolonged S-phase progression. Collectively, these findings indicate that ROCK1 exerts stage functions during MVC infection, promoting viral entry while limiting viral replication through regulation of cell-cycle progression. This dual role underscores the complex interplay between viral infection and host signaling pathways and provides mechanistic insights that may inform the development of host-directed antiviral strategies targeting ROCK1 signaling.

2026-02-11·mBio

Toxoplasma effector GRA15-driven CCL5 secretion enhances brain parasite load through microvascular sequestration of phagocytes

Article

作者: Afanaseva, Elena ; Rodriguez, Matias E. ; Barragan, Antonio

ABSTRACT:

Toxoplasma gondii exploits host phagocytes to disseminate systemically and establish infection in the central nervous system (CNS). Yet, the mechanisms governing the interaction between parasitized phagocytes and the brain endothelium remain elusive. Here, we show that T. gondii infection, but not parasite lysates, robustly induces transcriptional and secretory upregulation of the chemokine C–C motif ligand 5 (CCL5/RANTES) in primary brain endothelial cells and dendritic cells (DCs). This response was triggered by the parasite effector GRA15 through NF-κB signaling, while the effector TEEGR counteracted CCL5 induction in an MYR-translocon-dependent manner. In response to recombinant CCL5, infected DCs displayed increased hypermotility, chemotaxis toward CCL5 gradients, and enhanced transmigration across polarized endothelial monolayers. Intraperitoneally infected mice rapidly upregulated CCL5 in the blood and Ccl5 expression in the cerebral microvasculature, thereby increasing the adhesion of parasitized DCs and cerebral parasite loads. Pretreatment of mice with recombinant CCL5 dramatically elevated the sequestration of infected DCs, while treatment with the selective chemokine receptor 5 (CCR5) antagonist Maraviroc reverted sequestration. Together, these findings reveal that T. gondii co-opts the host CCL5/CCR5 axis via GRA15-mediated signaling to promote leukocyte-dependent dissemination and early colonization of the CNS.

IMPORTANCE:

The intracellular parasite Toxoplasma gondii invades immune cells to spread through the circulatory system, eventually reaching the brains of humans and animals. It is not well understood how parasitized immune cells interact with blood vessel walls, a process that ultimately helps Toxoplasma colonize the brain tissue. We found that when Toxoplasma infects the cells lining the blood vessels (endothelium), these produce C-C motif chemokine ligand 5 (CCL5), a potent signaling and attractant molecule. CCL5 production was triggered by a parasite-derived secreted protein, GRA15. CCL5 activated and attracted infected immune cells. In mice, the levels of CCL5 increased quickly in the brain microvasculature after infection, helping the infected immune cells adhere to brain vessels. When the effect of CCL5 was pharmacologically blocked, fewer infected cells sequestered in the brain vessels, lowering the parasite loads. These findings reveal a mechanism through which Toxoplasma manipulates host cells to produce factors that facilitate its colonization of the brain.

2026-02-01·PHYSIOLOGY & BEHAVIOR

Article

作者: Abiru, Memunat Diekololaoluwa ; Stringer, Amy D ; Wiah, Sonita ; Dachepalli, Meghana ; Rawls, Scott M ; Ruff, Michael R

RAP-103 is an orally active, multi-chemokine receptor antagonist (CRA) that inhibits three different chemokine receptors (CCR2, CCR5 and CCR8). Planarians, the simplest animals with bilateral symmetry and CNS cephalization, are useful for screening putative therapeutics because they express neurotransmitter systems and display mammalian-like behaviors when exposed to addictive drugs. We investigated effects of RAP-103 on spontaneous planarian behaviors (light avoidance, motility) and withdrawal responses associated with methamphetamine (METH) abstinence. Acute RAP-103 exposure decreased light avoidance (0.1, 1 μM) and increased motility (1 μM). For both endpoints, RAP-103 displayed an inverted U-shape concentration-effect curve. Maraviroc (1, 10 μM), a CCR5 antagonist, decreased light avoidance (like RAP-103) but reduced motility. RS 504393 (1, 10 μM), a CCR2 antagonist, increased light avoidance and reduced motility. For METH abstinence experiments, planarians were exposed for 5 min to a concentration of METH (1 μM) that did not cause spontaneous behaviors and then removed and placed into water. Planarians were then tested for light avoidance and motility during both early abstinence (0-5 min post-METH exposure) and later abstinence (15-20 min post-METH exposure). Light avoidance was enhanced during early METH abstinence whereas motility was reduced during later abstinence. RAP-103 (0.01, 0.1, 1 μM), administered during METH abstinence, counteracted METH-induced light avoidance but did not rescue METH-induced motility deficits. Our results with planarians show that RAP-103 displays anxiolytic-like and motor-enhancing effects and counteracts METH abstinence-induced behaviors, highlighting the potential of RAP-103 as a chemokine-based CNS therapeutic.

项与马拉韦罗相关的新闻（医药）

2026-01-20

·Pharmaceutical Technology

Shionogi expands ViiV Healthcare stake by $2.13bn as Pfizer sells up

ViiV Healthcare’s current product portfolio consists of 15 prescription HIV medicines. Image credit: T. Schneider via Shutterstock. As Pfizer sells its stake in ViiV Healthcare, Japan-based Shionogi & Co will increase its hold in the human immunodeficiency virus (HIV) medicines developer in a $2.13bn deal. ViiV Healthcare, which was established in a joint venture by GSK and Pfizer in 2009, will issue new shares to Shionogi for $2.13bn. The deal means Shionogi, which joined as shareholder in 2012, will increase its economic interest in ViiV Healthcare to 21.7%. The share issuance comes as Pfizer exits its 11.7% stake in ViiV Healthcare, marking an end to its involvement with the company. Pfizer will receive $1.89bn and GSK, which retains its 78.3% majority stake in ViiV Healthcare, will receive a special dividend of $250m. Shares in Tokyo-listed Shionogi rose 2.8% to Y2925 ($18.53) at market open on 20 January compared to market close of Y2840.5 on 19 January. ViiV Healthcare was established by Pfizer and GSK in a bid to combine resources to fight the global HIV pandemic. Both drugmakers transferred respective HIV assets to the company at the time, which included Epzicom/Kivexa (abacavir sulfate+lamivudine) and Selzentry/Celsentri (maraviroc). ViiV Healthcare’s current product portfolio consists of 15 prescription HIV medicines, with four candidates in clinical trials. The company is particularly seeking to develop ultra long-acting therapies for treatment and prevention or long-acting injectables that could be self-administered. This follows in a similar vein to Gilead’s Yeztugo (lenacapavir), the first and only biannual pre-exposure prophylaxis (PrEP) that won approval in the US and Europe in 2025. GlobalData Strategic Intelligence US Tariffs are shifting - will you react or anticipate? Don’t let policy changes catch you off guard. Stay proactive with real-time data and expert analysis. By GlobalData Learn more about Strategic Intelligence David Redfern, chair of ViiV Healthcare said: “This agreement simplifies ViiV’s shareholder structure and we look forward to continuing our highly successful collaboration with Shionogi to advance ViiV’s pipeline and portfolio of long-acting injectable HIV treatment and prevention medicines.” The current state of the HIV space The HIV space is heavily dominated by Gilead Sciences , especially since it announced data from the Phase III trial of its twice yearly PrEP medication Yeztugo. In Phase III trials, the twice-yearly drug showed near perfect efficacy, preventing nearly 100% of HIV cases in patients who received the study drug. The HIV market across the seven major markets (7MM: US, France, Germany, Italy, Spain, the UK, and Japan) is forecast to grow at a compound annual growth rate (CAGR) of 1.9% from $26.5bn in 2023 to $32.1bn in 2033, forecasts GlobalData . GlobalData is the parent company of Pharmaceutical Technology . In 2025, the World Health Organization (WHO) called for access expansion to newly approved human immunodeficiency virus (HIV) medication amid global funding cuts. A major hit to global HIV treatment efforts came in 2025 came when President Donald Trump cut a large amount of funding for foreign aid. This impacted HIV, malaria and tuberculosis treatment services in low-income countries supported by the United States Agency for International Development (USAID).

临床3期临床结果上市批准并购

2026-01-06

·中国生物器材网

从艾滋病毒到免疫疾病的新兴靶标：CCR5的结构、受体功能及应用

在人类与疾病斗争的漫长历史中，CCR5受体曾因艾滋病的出现而声名大噪——它曾是HIV入侵细胞的“关键钥匙”，也因此成为抗艾药物的重要靶点。然而，它的故事远不止于此。从基因编辑婴儿的伦理争议，到癌症免疫治疗的新希望，CCR5正在免疫与炎症疾病的广阔舞台上，展现其复杂而多面的生物学角色。一、CCR5受体结构 CC趋化因子受体5型（Chemokine receptor 5，CCR5）是一种主要表达于免疫细胞表面的G蛋白偶联受体。它能特异性结合趋化因子，从而在免疫监视和炎症反应中发挥核心作用，其配体包括CCL3、CCL4、CCL5、CCL7等。 CCR5受体由352个氨基酸残基组成，分子量约为40.6kDa，其结构包括胞外N末端、三个胞外环（EL1、EL2、EL3）、三个胞内环（IL1、IL2、IL3）、7个跨膜α螺旋和胞内C末端（如下图所示）。二、CCR5受体信号通路由CKLF1/CCR5、CCL5/CCR5等信号轴介导的炎症涉及MAPK、NF-κB、PI3K/Akt、mTOR、HIF-α及JAK-STAT多条关键信号通路。这些通路并非孤立运作，而是相互关联、协同作用，共同驱动炎症进程。 MAPK信号通路（见下图）：趋化因子 (如CCL3, CKLF1) → 结合并激活 CCR5 → ERK磷酸化 → 激活 RAS-ERK-MEK 通路，该通路是MAPK信号网络中的关键分支，这些级联反应共同驱动了CCR5介导的炎症过程。 NF-κB信号通路（见下图）：趋化因子 (如CKLF1, CCL5) → 结合并激活 CCR5 → 触发 NF-κB 释放与入核 → 启动炎症基因转录 PI3K/Akt/mTOR信号通路（见下图）： CCR5 被激活 → 磷酸化并激活 Akt → 同时解除对 mTOR 的抑制 → 协同驱动细胞生长、代谢等下游效应三、CCR5受体功能与相关疾病 CCR5是免疫细胞表面一种关键的“导航信号接收器”，其主要功能在于引导免疫细胞定向迁移至炎症或感染部位，并精准调控炎症反应的强度。与此同时，它也是HIV病毒入侵细胞所必需的主要共受体，其基因功能缺失（如CCR5-Δ32突变）可导致对HIV感染的天然耐受。基于这一双重角色，CCR5不仅成为抗艾滋病药物研发的经典靶点，其异常激活或表达也广泛参与多种疾病进程。因此，CCR5已成为连接感染、肿瘤、自身免疫及神经炎症等多个疾病领域的枢纽靶点，其药物研发也从单一的艾滋病治疗，拓展至癌症免疫联合治疗和炎症性疾病干预等广阔方向。 CCR5在中枢神经系统炎症疾病中的核心作用机制（如下图） CCR5是参与多种脑部疾病炎症过程的关键因子，其机制贯穿中风、阿尔茨海默病（AD）、帕金森病（PD）、癫痫、抑郁症和多发性硬化（MS）等疾病。针对其信号通路开发靶向疗法，有望为治疗上述神经系统疾病提供新的干预策略。 CCR5在非神经器官炎症疾病中的作用机制（如下图） CCR5是心脏、肝脏、肠道等多个器官炎症反应的关键共同介导因子。针对CCR5通路的靶向干预，有望为治疗心肌损伤、肝炎和IBD等疾病提供新的治疗策略。四、CCR5受体相关药物研发针对CCR5受体的药物研发，已经从单一的艾滋病治疗领域，扩展至癌症、肝脏及神经系统炎症等多个重要疾病方向。马拉韦罗 (Maraviroc)：它是首个也是目前唯一获批临床使用的CCR5靶向药。作为一种小分子拮抗剂，它通过“变形”CCR5受体来阻止HIV-1病毒侵入细胞。它专用于治疗仅感染“R5嗜性”HIV病毒的患者，是CCR5靶向疗法的基石。 Leronlimab (PRO 140)：这是一种人源化单克隆抗体，与受体结合力强、作用持久。它不仅被用于长效治疗HIV感染的临床试验，更在癌症治疗领域展现出巨大潜力。例如，它正被研究用于三阴性乳腺癌和结直肠癌，旨在通过阻断CCR5来改善肿瘤微环境、抑制转移。塞尼韦罗 (Cenicriviroc)：作为一种口服小分子双拮抗剂，它能同时抑制CCR2和CCR5这两个密切相关的受体。研发重点并非艾滋病，而是非酒精性脂肪性肝炎 (NASH) 等炎症纤维化疾病，旨在从源头抑制驱动疾病进展的炎症信号。格宁生物相关实验关于我们上海格宁生物科技有限公司（ScreeNingBio）成立于2020年，位于上海市浦江高科技园，专业提供生物医药研发外包服务，服务内容涵盖小分子和大分子药物研发早期阶段的多个方面，包括功能细胞株、药物筛选、高通量筛选、选择性和安全性评价、体外模型开发与验证、药物作用机理等。格宁生物不断自主开发新的药物靶点细胞株（如GPCR, Ion Channel）及各种药物筛选模型，全力打造筛选模型丰富、实验操作严谨、结果可信的药物筛选平台，为国内外医药企业提供优质高效的技术服务。联系我们电话：400-863-1023 邮箱：info@screeningbio.com 地址：上海市闵行区联航路1188号24号楼4层参考文献 Lin Y, Liu S, Sun Y, Chen C, Yang S, Pei G, Lin M, Yu J, Liu X, Wang H, Long J, Yan Q, Liang J, Yao J, Yi F, Meng L, Tan Y, Chen N, Yang Y, Ai Q. CCR5 and inflammatory storm. Ageing Res Rev. 2024 Apr;96:102286. doi: 10.1016/j.arr.2024.102286. Epub 2024 Mar 30. PMID: 38561044. Faivre N, Verollet C, Dumas F. The chemokine receptor CCR5: multi-faceted hook for HIV-1. Retrovirology. 2024 Jan 23;21(1):2. doi: 10.1186/s12977-024-00634-1. PMID: 38263120; PMCID: PMC10807162. Oppermann M. Chemokine receptor CCR5: insights into structure, function, and regulation. Cell Signal. 2004 Nov;16(11):1201-10. doi: 10.1016/j.cellsig.2004.04.007. PMID: 15337520.

2026-01-06

·格宁生物

CCR5：从艾滋病毒的必经之路，到免疫疾病的新兴靶标

在人类与疾病斗争的漫长历史中，CCR5受体曾因艾滋病的出现而声名大噪——它曾是HIV入侵细胞的“关键钥匙”，也因此成为抗艾药物的重要靶点。然而，它的故事远不止于此。从基因编辑婴儿的伦理争议，到癌症免疫治疗的新希望，CCR5正在免疫与炎症疾病的广阔舞台上，展现其复杂而多面的生物学角色。一、CCR5受体结构 CC趋化因子受体5型（Chemokine receptor 5，CCR5）是一种主要表达于免疫细胞表面的G蛋白偶联受体。它能特异性结合趋化因子，从而在免疫监视和炎症反应中发挥核心作用，其配体包括CCL3、CCL4、CCL5、CCL7等。 CCR5受体由352个氨基酸残基组成，分子量约为40.6kDa，其结构包括胞外N末端、三个胞外环（EL1、EL2、EL3）、三个胞内环（IL1、IL2、IL3）、7个跨膜α螺旋和胞内C末端（如下图所示）。二、CCR5受体信号通路由CKLF1/CCR5、CCL5/CCR5等信号轴介导的炎症涉及MAPK、NF-κB、PI3K/Akt、mTOR、HIF-α及JAK-STAT多条关键信号通路。这些通路并非孤立运作，而是相互关联、协同作用，共同驱动炎症进程。 MAPK信号通路（见下图）：趋化因子 (如CCL3, CKLF1) → 结合并激活 CCR5 → ERK磷酸化 → 激活 RAS-ERK-MEK 通路，该通路是MAPK信号网络中的关键分支，这些级联反应共同驱动了CCR5介导的炎症过程。 NF-κB信号通路（见下图）：趋化因子 (如CKLF1, CCL5) → 结合并激活 CCR5 → 触发 NF-κB 释放与入核 → 启动炎症基因转录 PI3K/Akt/mTOR信号通路（见下图）： CCR5 被激活 → 磷酸化并激活 Akt → 同时解除对 mTOR 的抑制 → 协同驱动细胞生长、代谢等下游效应三、CCR5受体功能与相关疾病 CCR5是免疫细胞表面一种关键的“导航信号接收器”，其主要功能在于引导免疫细胞定向迁移至炎症或感染部位，并精准调控炎症反应的强度。与此同时，它也是HIV病毒入侵细胞所必需的主要共受体，其基因功能缺失（如CCR5-Δ32突变）可导致对HIV感染的天然耐受。基于这一双重角色，CCR5不仅成为抗艾滋病药物研发的经典靶点，其异常激活或表达也广泛参与多种疾病进程。因此，CCR5已成为连接感染、肿瘤、自身免疫及神经炎症等多个疾病领域的枢纽靶点，其药物研发也从单一的艾滋病治疗，拓展至癌症免疫联合治疗和炎症性疾病干预等广阔方向。 CCR5在中枢神经系统炎症疾病中的核心作用机制（如下图） CCR5是参与多种脑部疾病炎症过程的关键因子，其机制贯穿中风、阿尔茨海默病（AD）、帕金森病（PD）、癫痫、抑郁症和多发性硬化（MS）等疾病。针对其信号通路开发靶向疗法，有望为治疗上述神经系统疾病提供新的干预策略。 CCR5在非神经器官炎症疾病中的作用机制（如下图） CCR5是心脏、肝脏、肠道等多个器官炎症反应的关键共同介导因子。针对CCR5通路的靶向干预，有望为治疗心肌损伤、肝炎和IBD等疾病提供新的治疗策略。四、CCR5受体相关药物研发针对CCR5受体的药物研发，已经从单一的艾滋病治疗领域，扩展至癌症、肝脏及神经系统炎症等多个重要疾病方向。马拉韦罗 (Maraviroc)：它是首个也是目前唯一获批临床使用的CCR5靶向药。作为一种小分子拮抗剂，它通过“变形”CCR5受体来阻止HIV-1病毒侵入细胞。它专用于治疗仅感染“R5嗜性”HIV病毒的患者，是CCR5靶向疗法的基石。 Leronlimab (PRO 140)：这是一种人源化单克隆抗体，与受体结合力强、作用持久。它不仅被用于长效治疗HIV感染的临床试验，更在癌症治疗领域展现出巨大潜力。例如，它正被研究用于三阴性乳腺癌和结直肠癌，旨在通过阻断CCR5来改善肿瘤微环境、抑制转移。塞尼韦罗 (Cenicriviroc)：作为一种口服小分子双拮抗剂，它能同时抑制CCR2和CCR5这两个密切相关的受体。研发重点并非艾滋病，而是非酒精性脂肪性肝炎 (NASH) 等炎症纤维化疾病，旨在从源头抑制驱动疾病进展的炎症信号。格宁生物相关实验关于我们上海格宁生物科技有限公司（ScreeNingBio）成立于2020年，位于上海市浦江高科技园，专业提供生物医药研发外包服务，服务内容涵盖小分子和大分子药物研发早期阶段的多个方面，包括功能细胞株、药物筛选、高通量筛选、选择性和安全性评价、体外模型开发与验证、药物作用机理等。格宁生物不断自主开发新的药物靶点细胞株（如GPCR, Ion Channel）及各种药物筛选模型，全力打造筛选模型丰富、实验操作严谨、结果可信的药物筛选平台，为国内外医药企业提供优质高效的技术服务。联系我们电话：400-863-1023 邮箱：info@screeningbio.com 地址：上海市闵行区联航路1188号24号楼4层参考文献 [1]Lin Y, Liu S, Sun Y, Chen C, Yang S, Pei G, Lin M, Yu J, Liu X, Wang H, Long J, Yan Q, Liang J, Yao J, Yi F, Meng L, Tan Y, Chen N, Yang Y, Ai Q. CCR5 and inflammatory storm. Ageing Res Rev. 2024 Apr;96:102286. doi: 10.1016/j.arr.2024.102286. Epub 2024 Mar 30. PMID: 38561044. [2]Faivre N, Verollet C, Dumas F. The chemokine receptor CCR5: multi-faceted hook for HIV-1. Retrovirology. 2024 Jan 23;21(1):2. doi: 10.1186/s12977-024-00634-1. PMID: 38263120; PMCID: PMC10807162. [3]Oppermann M. Chemokine receptor CCR5: insights into structure, function, and regulation. Cell Signal. 2004 Nov;16(11):1201-10. doi: 10.1016/j.cellsig.2004.04.007. PMID: 15337520.

免疫疗法临床申请

100 项与马拉韦罗相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D06670	马拉韦罗	J05AX09	DB04835

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
HIV感染	美国	ViiV Healthcare Co.	2007-08-06

未上市

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
脂肪肝	临床3期	英国	ViiV Healthcare Ltd.	2017-03-01
代谢功能障碍相关的脂肪肝病	临床3期	英国	ViiV Healthcare Ltd.	2017-03-01
艾滋病痴呆复合征	临床3期	美国	ViiV Healthcare Ltd.	2015-06-01
心血管疾病	临床3期	美国	Pfizer Inc.	2010-01-01
炎症	临床3期	美国	Pfizer Inc.	2010-01-01
获得性免疫缺陷综合征	临床3期	瑞典	Pfizer Ltd.	2004-12-22
新型冠状病毒感染	临床2期	西班牙	ViiV Healthcare Ltd.	2020-06-26
艾滋病相关性卡波西肉瘤	临床2期	美国	Pfizer Inc.	2011-03-09
艾滋病相关性卡波西肉瘤	临床2期	美国	ViiV Healthcare Ltd.	2011-03-09
GM1神经节苷脂贮积病	临床2期	西班牙	-	2009-02-23

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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


NCT05932550 (Pubmed)	临床2期	抑郁症追加 CCR5	10	Maraviroc 300 mg	醖築築衊鏇鬱鑰鏇鏇窪(衊選襯鏇淵鏇鹹製膚簾) = 製鑰憲憲鹽壓簾構夢積製簾築網憲蓋艱製築鹹 (簾鏇積鹽膚艱壓醖壓廠, 9.3)	积极	2024-06-06
NCT02881762 (MAVERIC, CTgov)	临床4期	HIV感染 \| 丙型肝炎	10	Maraviroc (Maraviroc)	獵窪遞築襯糧夢選繭餘(構鹽齋夢獵選壓餘鏇衊) = 醖餘餘廠蓋窪網齋簾鑰壓積構蓋夢鏇醖醖鏇淵 (窪淵醖壓窪觸壓簾淵築, 1012880) 更多	-	2024-05-01
				Maraviroc (No Maraviroc)	獵窪遞築襯糧夢選繭餘(構鹽齋夢獵選壓餘鏇衊) = 鑰蓋積獵鹹獵淵餘網網壓積構蓋夢鏇醖醖鏇淵 (窪淵醖壓窪觸壓簾淵築, 1411027) 更多
NCT04435522 (CTgov)	临床1期	新型冠状病毒感染	9	maraviroc	衊構憲醖鹹築鏇鹽餘壓 = 鑰範艱鏇遞襯憲餘構願鹹艱襯觸獵構範遞獵糧 (構糧繭衊鑰鹹餘齋夢壓, 襯廠膚糧襯繭淵夢範鹹 ~ 艱壓鬱鬱憲糧網糧選鑰) 更多	-	2024-04-29
NCT02741323 (CTgov)	临床2期	肾脏疾病 \| HIV感染	97	maraviroc (Arm 1: Maraviroc (MVC))	選觸選憲憲積願簾廠繭(糧廠鬱壓鬱廠簾繭憲鹹) = 獵蓋淵鑰淵襯窪襯選繭齋鑰蓋鬱壓夢廠憲鏇鑰 (艱積夢網衊憲蓋繭艱淵, 繭糧艱淵獵鏇願遞憲遞 ~ 醖範艱繭願夢窪鑰顧築) 更多	-	2023-08-21
				Placebo (Arm 2: Placebo)	選觸選憲憲積願簾廠繭(糧廠鬱壓鬱廠簾繭憲鹹) = 獵簾構憲蓋遞憲選醖壓齋鑰蓋鬱壓夢廠憲鏇鑰 (艱積夢網衊憲蓋繭艱淵, 網窪繭餘襯夢築鬱選醖 ~ 網獵蓋憲繭憲艱鑰鑰蓋) 更多
NCT00948753 (CTgov)	临床1/2期	造血干细胞移植 \| 移植物抗宿主病	38	Maraviroc 150 MG (Phase 1: 150mg Maraviroc)	齋衊壓衊衊鏇顧築廠憲 = 鑰憲願願築鏇艱膚衊憲繭糧憲鹹顧構夢觸鹽襯 (壓鏇膚鑰範願鹽鏇觸淵, 顧淵選醖觸繭選繭糧遞 ~ 窪積築遞齋餘艱獵夢顧) 更多	-	2022-05-17
				Maraviroc 300 mg (Phase 1: 300mg Maraviroc)	齋衊壓衊衊鏇顧築廠憲 = 鹹廠夢糧獵鬱廠鏇構製繭糧憲鹹顧構夢觸鹽襯 (壓鏇膚鑰範願鹽鏇觸淵, 憲鏇壓選網齋繭醖簾選 ~ 衊糧網簾膚積築製網糧) 更多
NCT02519777 (CTgov)	临床4期	认知功能障碍 \| HIV感染	191	Placebo for dolutegravir (DTG) (Arm A: Placebo MVC and Placebo DTG)	餘廠鑰醖鹹憲齋觸餘網(鬱鬱遞蓋鏇網遞膚選簾) = 餘鬱鹽鹽鏇範積築製糧繭夢壓餘醖願蓋廠壓築 (餘鹽醖鑰選顧夢構鹽壓, 壓鏇範鏇廠獵襯鑰淵夢 ~ 壓艱鹽築鏇範積選繭顧) 更多	-	2022-03-02
				Placebo for maraviroc (MVC)+Dolutegravir (DTG) (Arm B: DTG and Placebo MVC)	餘廠鑰醖鹹憲齋觸餘網(鬱鬱遞蓋鏇網遞膚選簾) = 艱願鹽遞艱窪醖窪憲淵繭夢壓餘醖願蓋廠壓築 (餘鹽醖鑰選顧夢構鹽壓, 觸夢鏇顧襯積構網築衊 ~ 繭積選觸膚選鏇夢餘艱) 更多
NCT03172026 (MAROS, CTgov)	临床2/3期	脑卒中	2	Rehabilitation therapy+Maraviroc 300 mg (Maraviroc + Augmented Rehabilitation)	獵膚觸壓築簾憲壓獵積(餘鏇顧鑰憲壓繭鏇鑰壓) = 獵顧衊衊範範願膚積廠網鬱餘糧築衊艱糧構襯 (廠憲壓鑰餘鬱遞簾憲顧, 壓築網鹹淵繭構憲鹽範 ~ 醖選遞鏇膚蓋醖顧夢鏇) 更多	-	2021-08-03
				Placebo 300 mg (Placebo + Augmented Rehabilitation)	獵膚觸壓築簾憲壓獵積(餘鏇顧鑰憲壓繭鏇鑰壓) = 艱鏇願願壓築鏇築願壓網鬱餘糧築衊艱糧構襯 (廠憲壓鑰餘鬱遞簾憲顧, 製蓋齋鹹範遞範醖糧鑰 ~ 願餘鑰積獵齋鹽積築夢) 更多
NCT03274804 (PICCASSO, CTgov)	临床1期	脊髓小脑变性 \| 转移性微卫星稳定结直肠癌 \| 转移性结直肠癌	20	Pembrolizumab+maraviroc	獵觸顧選鏇鏇鹹壓築範 = 夢壓廠網鬱積顧鬱選範糧鏇製艱製艱鏇遞窪襯 (壓繭膚鏇簾遞齋鏇鏇夢, 糧築憲遞製網淵艱顧鏇 ~ 鹽積積範網鏇鏇願構襯) 更多	-	2021-04-22
NCT01276236 (CTgov)	临床2期	艾滋病相关性卡波西肉瘤	13	maraviroc	遞範膚鑰製簾簾糧構壓 = 鹽鏇鬱齋構獵獵網衊築願衊膚網憲餘衊襯窪鬱 (憲窪觸醖築獵齋鬱鏇憲, 鹽艱糧鹽醖鏇簾願餘繭 ~ 壓鹹齋齋膚糧醖襯壓網) 更多	-	2021-03-05
NCT01785810 (CTgov)	临床2期	急性髓性白血病 \| 慢性淋巴细胞白血病 \| 急性淋巴细胞白血病 ... 更多	37	Maraviroc 300 mg	糧餘鹹衊築顧觸醖選艱 = 蓋夢鬱廠築構願鹹遞簾鏇範構選範選蓋範鬱艱 (餘糧積繭艱願窪網構艱, 簾遞襯鏇鏇簾襯鬱選鹹 ~ 壓選壓襯醖齋鑰遞窪醖) 更多	-	2021-01-11