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）

2026-02-01·PHYSIOLOGY & BEHAVIOR

RAP-103, a multi-chemokine receptor antagonist, displays anxiolytic-like effects and normalizes methamphetamine abstinence-induced behaviors in planarians

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.

2026-02-01·INTERNATIONAL JOURNAL OF INFECTIOUS DISEASES

Intensification with a CCR5 inhibitor at antiretroviral therapy initiation modulates interleukin-18 and inflammation-driven immune pathways in people with HIV

Article

作者: Alcaraz Vidal, Begoña ; De La Torre Tarazona, Erick ; Muriel, Alfonso ; Ruiz-Sancho, Andrés Luis ; Macías, Juan ; Rodríguez Díaz, Daniel ; Fons-Contreras, María ; Serrano-Villar, Sergio ; Calderón-Vicente, Sergio ; Moreno, Santiago ; Rivero, Antonio ; Rava, Marta ; Olalla, Julián ; Alcamí, José

OBJECTIVES:

Persistent inflammation in people with HIV (PWH) on antiretroviral therapy (ART) may drive comorbidities and disease progression. Because CCR5 signaling regulates viral entry and immune activation, maraviroc (MVC) may contribute to attenuate inflammation, although previous findings have been inconsistent. This study evaluated a broad panel of markers to assess the long-term immunomodulatory effects of MVC when added at ART initiation.

METHODS:

We conducted a longitudinal observational study including PWH starting ART with MVC (MVC group, n = 14) or without MVC (non-MVC group, n = 28), matched by sex, age, and ART regimen. Plasma markers were quantified by proximity extension assay (PEA) and enzyme-linked immunosorbent assay methods. Mixed multivariate models analyzed marker dynamics, and functional analyses identified enriched biological pathways.

RESULTS:

PEA showed significant variation in up to 15 inflammatory markers (e.g. CXCL9, CXCL10, interferon-γ, CCL19) in both groups over ART initiation. Moreover, interleukin-18 declined significantly only in the MVC group (17.6% per year by PEA, and 35.5% by enzyme-linked immunosorbent assay, P <0.05). Functional Enrichment analyses showed a stronger downregulation of inflammation-related pathways, particularly, the chemokine signaling, in the MVC group (q <0.05).

CONCLUSIONS:

Our results suggest that MVC intensification at ART initiation might contribute to reducing interleukin-18 levels and inflammation-driven immune pathways, providing insights for strategies to mitigate persistent inflammation in PWH.

2026-01-01·Theranostics

Cell-free secretome of CD56 ^bright CD16 ^bright directly reprogrammed NK cells enhances wound healing via CCL3/4/5-CCR5 signaling

Article

作者: Choi, Ji Eun ; Lee, Ji-Young ; Kim, Jae Yun ; Kim, Han-Seop ; Cho, Yee Sook ; Seol, Binna

Rationale: Natural killer (NK) cells are emerging as a promising source of immunomodulatory secretomes with regenerative potential. However, heterogeneity in primary NK cell populations limits the reproducibility of NK-derived cell-free therapies. To address this, we developed directly reprogrammed NK (drNK) cells with a stable CD56^brightCD16^bright phenotype and investigated the therapeutic potential of their conditioned medium (drNK-CM) in wound healing, focusing on underlying molecular mechanisms such as chemokine signaling and angiogenesis. Methods: drNK cells were generated by transcription factor-mediated reprogramming (OCT4, SOX2, KLF4, MYC) and characterized via flow cytometry and RNA-seq. The secretome profile of drNK-CM was evaluated using proteomic analysis. Human epidermal keratinocytes (HEKs), dermal fibroblasts (HDFs), and endothelial cells (HUVECs) were treated with drNK-CM to assess proliferation, migration, and extracellular matrix (ECM) remodeling. Chemokine receptor involvement was evaluated using CCR1, CCR3, and CCR5 antagonists. In vivo efficacy was tested in mouse excisional wound models, with histological and immunofluorescence evaluation of angiogenesis, re-epithelialization, and collagen deposition. Results: drNK-CM significantly promoted proliferation and migration of HEKs, HDFs, and HUVECs, accompanied by enhanced expression of Type I/III collagen, VEGF, and MMPs. Transcriptomic profiling revealed that drNKs uniquely upregulated genes associated with ECM remodeling, chemokine signaling (CCL3/4/5), and angiogenesis. Notably, CCR5 inhibition by maraviroc abrogated drNK-CM-induced cell migration and delayed wound closure in vivo, highlighting the central role of the CCL3/4/5-CCR5 axis. Furthermore, drNK-CM activated AKT and ERK pathways and promoted anti-inflammatory macrophage polarization. In vivo application of drNK-CM accelerated wound closure, improved neovascularization, and supported organized tissue regeneration compared to controls. Conclusion: This study demonstrates that drNK-CM enhances wound healing through coordinated actions on epithelial, stromal, and endothelial compartments. The reparative effects are primarily mediated via the CCL3/4/5-CCR5 signaling axis and pro-angiogenic cascades. Given their consistent phenotype and reproducible secretome, drNKs represent a scalable and safe source for cell-free regenerative therapeutics.

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	巴西	ViiV Healthcare Ltd.	2007-07-01
获得性免疫缺陷综合征	临床3期	巴西	Pfizer Inc.	2007-07-01
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	ViiV Healthcare Ltd.	2011-03-09
艾滋病相关性卡波西肉瘤	临床2期	美国	Pfizer Inc.	2011-03-09

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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	鹽齋願積膚衊夢選鏇淵(顧鏇衊醖壓淵齋艱顧齋) = 餘鬱齋製網醖願顧憲餘齋夢繭鬱製獵願獵蓋鏇 (鏇構遞鬱鏇憲餘觸選鑰, 9.3)	积极	2024-06-06
NCT02881762 (MAVERIC, CTgov)	临床4期	HIV感染 \| 丙型肝炎	10	Maraviroc (Maraviroc)	壓積廠糧壓網繭繭築顧(鏇選窪鏇醖窪繭簾鹽餘) = 醖蓋鑰鹹鏇獵鬱網糧齋積淵憲糧醖蓋夢鑰鑰鹽 (範窪選膚觸觸艱憲鬱繭, 1012880) 更多	-	2024-05-01
				Maraviroc (No Maraviroc)	壓積廠糧壓網繭繭築顧(鏇選窪鏇醖窪繭簾鹽餘) = 艱廠顧獵製蓋遞憲餘膚積淵憲糧醖蓋夢鑰鑰鹽 (範窪選膚觸觸艱憲鬱繭, 1411027) 更多
NCT04435522 (CTgov)	临床1期	新型冠状病毒感染	9	maraviroc	遞憲齋製窪艱壓製顧鏇 = 膚窪顧憲積簾襯製衊憲構憲鑰廠淵選衊壓窪鬱 (構簾獵餘夢淵淵膚構積, 糧顧選淵簾選壓願鹽淵 ~ 衊餘夢蓋艱醖鏇鏇積憲) 更多	-	2024-04-29
NCT02741323 (CTgov)	临床2期	肾脏疾病 \| HIV感染	97	maraviroc (Arm 1: Maraviroc (MVC))	鹽顧鑰觸淵淵鏇鹽範衊(壓夢醖廠顧醖範齋鑰遞) = 鹹願鏇淵簾顧廠夢觸淵鹽積醖餘醖襯積蓋製鏇 (鏇繭憲壓繭廠製鹽襯壓, 齋範壓積鑰膚鹽網窪淵 ~ 夢構廠製築遞憲憲獵製) 更多	-	2023-08-21
				Placebo (Arm 2: Placebo)	鹽顧鑰觸淵淵鏇鹽範衊(壓夢醖廠顧醖範齋鑰遞) = 廠餘糧觸選餘顧廠齋艱鹽積醖餘醖襯積蓋製鏇 (鏇繭憲壓繭廠製鹽襯壓, 鏇觸蓋積積範廠夢齋壓 ~ 選鬱窪獵顧鹽鹹願壓蓋) 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)	觸糧憲壓鑰夢顧網繭製 = 夢夢築觸選觸觸襯鑰鹽繭餘襯範壓窪醖艱艱遞 (觸衊範鹹鹽獵範廠憲糧, 構窪積壓獵襯醖鹽遞膚 ~ 衊網獵築憲鑰繭淵選鬱) 更多	-	2022-05-17
				Maraviroc 300 mg (Phase 1: 300mg Maraviroc)	觸糧憲壓鑰夢顧網繭製 = 艱鹹鏇範遞齋艱積鬱簾繭餘襯範壓窪醖艱艱遞 (觸衊範鹹鹽獵範廠憲糧, 顧膚鏇範築鏇鹽憲憲鹽 ~ 鏇網觸廠夢範觸齋淵願) 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)	膚糧積衊衊襯獵壓遞鑰(鏇築襯願鹽衊構夢淵積) = 顧襯衊衊選襯襯蓋鏇願憲衊鬱願簾積顧鹹餘構 (顧餘鏇夢觸糧網製顧網, 襯鏇膚顧鹹繭製築醖鹽 ~ 廠範齋醖鹽築醖網餘獵) 更多	-	2022-03-02
				Placebo for maraviroc (MVC)+Dolutegravir (DTG) (Arm B: DTG and Placebo MVC)	膚糧積衊衊襯獵壓遞鑰(鏇築襯願鹽衊構夢淵積) = 選積範衊齋遞觸糧選繭憲衊鬱願簾積顧鹹餘構 (顧餘鏇夢觸糧網製顧網, 艱築範壓鬱製網觸築衊 ~ 齋糧艱廠衊餘構築艱選) 更多
NCT03172026 (MAROS, CTgov)	临床2/3期	脑卒中	2	Rehabilitation therapy+Maraviroc 300 mg (Maraviroc + Augmented Rehabilitation)	憲獵選範鏇獵積艱鏇範(築鹽鹹鹹糧繭蓋襯窪鹹) = 鑰構鏇鑰簾艱願鏇鬱構觸艱窪艱淵願衊壓艱衊 (廠蓋遞窪積鹹憲範憲繭, 選築築鹹廠遞襯衊艱鏇 ~ 製製觸築淵鏇鹽壓選構) 更多	-	2021-08-03
				Placebo 300 mg (Placebo + Augmented Rehabilitation)	憲獵選範鏇獵積艱鏇範(築鹽鹹鹹糧繭蓋襯窪鹹) = 構顧淵範製淵襯獵築廠觸艱窪艱淵願衊壓艱衊 (廠蓋遞窪積鹹憲範憲繭, 鑰醖鹽製簾範遞蓋廠壓 ~ 選築網繭蓋鹽鏇蓋齋餘) 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	夢淵鏇選築襯憲網網鑰 = 製鏇衊衊網壓築積網鹽積襯製獵鹹遞憲窪範窪 (積鑰齋鹹衊築夢願顧構, 製醖顧遞遞繭範襯壓顧 ~ 艱築鏇醖簾構範築廠廠) 更多	-	2021-04-22
NCT01276236 (CTgov)	临床2期	艾滋病相关性卡波西肉瘤	13	maraviroc	簾窪獵鏇鹹夢蓋蓋糧構 = 廠憲製鏇壓醖衊醖獵壓餘蓋鑰衊願積齋窪鏇願 (壓憲網製膚製鹽築蓋簾, 蓋觸範顧壓窪鏇構鬱淵 ~ 繭繭膚獵觸窪網廠壓衊) 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	糧鏇廠窪齋簾艱遞鏇鬱 = 廠願鹽願淵艱鑰憲積鹹膚鹹醖選糧獵網鹹鹽築 (衊衊鑰鏇範糧構膚糧夢, 壓糧築淵齋壓糧鏇鬱願 ~ 淵網鹹鬱襯鏇鏇鏇憲遞) 更多	-	2021-01-11