马拉韦罗(Maraviroc) - 药物靶点：CCR5_在研适应症：HIV感染，新冠肺炎后遗症，痴呆_专利_临床

概要

基本信息

药物类型

小分子化药

别名

Maraviroc (JAN/INN)、MVC、UK-427857

+ [4]

靶点

CCR5

作用方式

拮抗剂

作用机制

CCR5拮抗剂(C-C趋化因子受体5型拮抗剂)

治疗领域

免疫系统疾病感染泌尿生殖系统疾病+ [4]

在研适应症

HIV感染新冠肺炎后遗症痴呆+ [1]

非在研适应症

获得性免疫缺陷综合征艾滋病痴呆复合征艾滋病相关性卡波西肉瘤+ [9]

原研机构

ViiV Healthcare Ltd.

在研机构

晖致制药（大连）有限公司ViiV Healthcare BVHealthBioAI

+ [3]

非在研机构

Pfizer Inc.

GSK Plc

权益机构-

最高研发阶段批准上市

首次获批日期

美国 (2007-08-06),

HIV感染

最高研发阶段(中国)批准上市

特殊审评-

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结构/序列

分子式C29H41F2N5O

InChIKeyGSNHKUDZZFZSJB-QYOOZWMWSA-N

CAS号376348-65-1

关联

160

项与马拉韦罗相关的临床试验

NCT06853223

/ Recruiting临床2期IIT

A Randomized Trial of CCR5 Inhibition as a Complement to Lung Transplant Induction Immunosuppression

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]

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-

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]

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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1,590

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.

2026-03-04·JOURNAL OF BIOMOLECULAR STRUCTURE & DYNAMICS

Article

作者: Murahari, Manikanta ; Simon, Mugisa ; Prasad, Burra V. L. S. ; Derrick, Ssebaduka ; Bhadra, Pratiti ; Sahoo, Partha Sarathi ; Dyvapu, Lalitha Bhaskarani

The CC chemokine receptor 5 (CCR5) is the principal entry receptor for HIV1 (macrophage tropic) as observed in the early stages of viral replication during attachment to the host cell. The coreceptor switch is one of the possible mechanisms for viral resistance. Hence, molecules designed to bind and inhibit CCR5 or CXCR4 would be effective in HIV (human immunodeficiency virus) therapy to prevent entry of the virus, stop further infection of cells, and allow time for its clearance from the body (through immunity intervention). The aim of this study was to design effective and safer CCR5 coreceptor antagonists. Two ligand-based pharmacophore models were generated with drugs in market and clinical trials using PharmGist tool. The model was utilized to screen the ZINC database to obtain compounds with the required features and proceed for docking with AutoDock tools. Top ten compounds with good docking score and significant interactions at the active pocket were advanced to ADME (absorption, distribution, metabolism, and excretion) and toxicity predictions. Interestingly, ZINC08948076 (Mol1) and ZINC08966180 (Mol2) share similar molecular fingerprints with the drug molecule, BMS-813160. In contrast, the MD simulation trajectories revealed ZINC13150285 (Mol3) and maraviroc to have similar conformational dynamics (RMSD and Rg) between the ligand and the target protein. Additionally, ZINC24968598 (Mol4) was observed to have the lowest potential energy and ZINC09515758 (Mol5) with the lowest interaction energy. Overall, the study could identify ZINC09515758 and ZINC00673808 as potential hit molecules for further experimental investigation.

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.

47

项与马拉韦罗相关的新闻（医药）

2026-03-31

·百度百家

「AACR 2026」GPCR靶点盘点：从CXCR4到GPRC5D，哪些方向正在走热？

在肿瘤创新药研发中，G蛋白偶联受体（GPCR）一直是一个有些尴尬的靶点家族。从成药史来看，它是最成熟的一类药物靶点；但从肿瘤新药版图来看，GPCR又长期没有HER2、TROP2、CLDN18.2这类靶点那么显眼。不过，从AACR 2026的摘要趋势来看，这种局面正在发生变化。本届会议上，GPCR相关项目已经明显从传统小分子受体调控，延伸到肿瘤微环境、Treg清除、ADC、双抗、多特异性分子以及放射性药物等多个方向。尤其是CXCR4、SSTR2、CCR8、LGR5、GPRC5D、CCR5等靶点，不仅摘要露出相对集中，而且已经出现较清晰的产品化和平台化开发路径。 1、CXCR4：成熟靶点仍在迭代，转移与微环境价值持续放大在GPCR靶点中，CXCR4依然是最成熟、也最接近临床转化的一类。它在肿瘤中的价值主要围绕细胞迁移、骨髓归巢、转移、耐药和微环境重塑展开，因此既有基础研究深度，也有较强的临床延展性。AACR 2026上，CXCR4的关注点已经从“做不做这个靶点”进一步转向为“如何做患者分层、如何进入联合治疗，以及如何挖掘更明确的应答人群”。从本届摘要来看，CXCR4方向既有Motixafortide这类明确分子的临床转化信号，也有TNX-1700这样的新项目线索，说明这一靶点仍然处于持续活跃状态。代表性摘要包括： CXCR4作用机制及药物研究进展 2、SSTR2：从核药标杆靶点，走向更广义的偶联平台靶点在GPCR家族中，SSTR2是最具“核药属性”的代表靶点之一。过去提到SSTR2，首先想到的通常是神经内分泌肿瘤和放射配体治疗；但AACR 2026显示，这个靶点的开发边界正在快速拓宽，已经不再局限于传统的显像或核素治疗，而是明显延伸到肽偶联药物、双特异性ADC以及新型放射性偶联药物。从布局主体看，Italfarmaco、基石药业、上海核舟医药都带来了明确项目线索，说明SSTR2正在从“经典核药靶点”逐步演变成一个更广义的偶联递送平台靶点。代表性摘要包括： 3、CCR8：Treg清除赛道持续升温，免疫抑制微环境成为核心切口如果说本届AACR上哪个GPCR靶点最能体现“肿瘤免疫新方向”，那CCR8一定是重点之一。CCR8与肿瘤浸润性调节性T细胞（Treg）高度相关，因此天然适合作为肿瘤免疫抑制微环境改造的切入点。相比传统免疫激活逻辑，CCR8更强调定向清除肿瘤相关Treg，这也是它快速升温的重要原因。从今年AACR的摘要看，CCR8已经出现较完整的开发梯队：既有去除型抗体的分子特征研究，也有一期临床结果，甚至开始向ADC方向延展。布局主体包括Kainova Therapeutics、Amgen、Takeda，产业化信号已经比较明确。代表性摘要包括： 4、LGR5：从肿瘤干细胞标志物，走向ADC与双抗开发靶点 LGR5是一个典型的“生物学意义先行、药物开发逐步跟上”的靶点。它长期与肿瘤干细胞、耐药和复发相关，因此早年更多出现在机制研究中。但从AACR 2026的信号来看，LGR5正在快速摆脱“只适合做文章”的印象，转向更实在的抗体药物开发阶段。这次会议里，LGR5方向已经出现LGR5靶向ADC、EGFRxLGR5双抗、VHH抗体等多种策略，说明它正在成为实体瘤中值得重新评估的可药物化靶点。企业层面，Dragon Boat Biopharmaceutical的项目推进最为直接。代表性摘要包括： 5、GPRC5D：骨髓瘤赛道里最具热度的GPCR靶点之一在血液瘤领域，GPRC5D已经成为继BCMA之后极具关注度的新一代靶点之一。尤其是在多发性骨髓瘤中，GPRC5D为复发难治患者提供了新的靶向维度，也因此成为多特异性抗体和T-cell engager开发中的重点对象。AACR 2026上，这一靶点已经不再只是概念验证，而是明显进入了平台竞争与分子设计优化阶段。从摘要看，GPRC5D方向既有Talquetamab相关临床应用背景，也有多特异性抗体和多价多特异性ADC的新设计。相关布局主体包括Integral Molecular和Synthetic Design Lab，显示这一靶点正在进入“谁能做得更优”的竞争阶段。代表性摘要包括： 6、CCR5：老靶点正在被重新激活，联合治疗价值值得重估和前面几个靶点相比，CCR5并不是一个“新方向”。它在炎症、病毒感染和免疫迁移领域早已被广泛研究，因此很多人对它的第一印象甚至不是肿瘤。但AACR 2026的一些摘要提示，CCR5在肿瘤中的开发空间远未被挖尽，尤其是在联合治疗、微环境调控和适应症拓展上仍有不少机会。这次会议中，CCR5相关线索主要围绕leronlimab和maraviroc等已有分子的再利用展开，体现出典型的“老靶点新场景”特征。对于希望寻找机制成熟、转化路径相对清晰的团队来说，CCR5仍然值得持续关注。代表性摘要包括： 7、CXCR2：肿瘤炎症轴的关键节点，适合与免疫和微环境策略联动在本届AACR中，CXCR2的摘要数量不算最多，但研究方向非常集中，几乎都围绕IL-8、中性粒细胞募集、肿瘤炎症和休眠细胞唤醒展开。这类靶点的价值不在于单纯作用于肿瘤细胞，而在于它连接了肿瘤与髓系免疫系统之间的通讯网络，因此很适合与免疫治疗、炎症阻断和耐药微环境调控联动。从企业化线索看，虽然本次会议上披露的成熟项目不算多，但AZD5069等已有分子仍然给出了较明确的转化方向。代表性摘要包括： 8、DRD1：神经递质受体在肿瘤中的角色，正从边缘走向前沿如果说前面的几个靶点已经更接近“产品开发逻辑”，那么DRD1更像是本届AACR中一个值得前瞻关注的信号。作为多巴胺受体家族成员，DRD1传统上并不属于肿瘤药物开发的核心靶点，但这次多篇摘要将其与EZH2、表观遗传调控和三阴性乳腺癌进展联系起来，提示神经递质信号和肿瘤表观遗传之间的交叉正在被重新认识。目前这一方向仍以前沿研究为主，产业化布局还不密集，但恰恰因为处于早期，更值得被持续跟踪。代表性摘要包括：回看AACR 2026，可以非常明显地感受到，GPCR已经不再只是传统小分子药物的主场。在肿瘤领域，越来越多的GPCR靶点正在进入抗体、ADC、双抗、放射性药物和免疫微环境重塑的开发体系。其中，CXCR4、CCR8、CCR5、CXCR2更偏向免疫与微环境调控；SSTR2代表的是核药与偶联药物的持续融合；而LGR5、GPRC5D则更像是GPCR靶点走向抗体工程、多特异性分子和ADC开发的标志性案例。如果说过去行业对GPCR的判断还是“肿瘤里有机会，但不算主流”，那么从今年AACR的趋势看，至少一部分GPCR靶点，已经开始真正进入主流创新药视野。

2026-03-31

·有驾

「AACR 2026」GPCR靶点盘点：从CXCR4到GPRC5D，哪些方向正在走热？

在肿瘤创新药研发中，G蛋白偶联受体（GPCR）一直是一个有些尴尬的靶点家族。从成药史来看，它是最成熟的一类药物靶点；但从肿瘤新药版图来看，GPCR又长期没有HER2、TROP2、CLDN18.2这类靶点那么显眼。不过，从AACR 2026的摘要趋势来看，这种局面正在发生变化。本届会议上，GPCR相关项目已经明显从传统小分子受体调控，延伸到肿瘤微环境、Treg清除、ADC、双抗、多特异性分子以及放射性药物等多个方向。尤其是CXCR4、SSTR2、CCR8、LGR5、GPRC5D、CCR5等靶点，不仅摘要露出相对集中，而且已经出现较清晰的产品化和平台化开发路径。 1、CXCR4：成熟靶点仍在迭代，转移与微环境价值持续放大在GPCR靶点中，CXCR4依然是最成熟、也最接近临床转化的一类。它在肿瘤中的价值主要围绕细胞迁移、骨髓归巢、转移、耐药和微环境重塑展开，因此既有基础研究深度，也有较强的临床延展性。AACR 2026上，CXCR4的关注点已经从“做不做这个靶点”进一步转向为“如何做患者分层、如何进入联合治疗，以及如何挖掘更明确的应答人群”。从本届摘要来看，CXCR4方向既有Motixafortide这类明确分子的临床转化信号，也有TNX-1700这样的新项目线索，说明这一靶点仍然处于持续活跃状态。代表性摘要包括： CXCR4作用机制及药物研究进展 2、SSTR2：从核药标杆靶点，走向更广义的偶联平台靶点在GPCR家族中，SSTR2是最具“核药属性”的代表靶点之一。过去提到SSTR2，首先想到的通常是神经内分泌肿瘤和放射配体治疗；但AACR 2026显示，这个靶点的开发边界正在快速拓宽，已经不再局限于传统的显像或核素治疗，而是明显延伸到肽偶联药物、双特异性ADC以及新型放射性偶联药物。从布局主体看，Italfarmaco、基石药业、上海核舟医药都带来了明确项目线索，说明SSTR2正在从“经典核药靶点”逐步演变成一个更广义的偶联递送平台靶点。代表性摘要包括： 3、CCR8：Treg清除赛道持续升温，免疫抑制微环境成为核心切口如果说本届AACR上哪个GPCR靶点最能体现“肿瘤免疫新方向”，那CCR8一定是重点之一。CCR8与肿瘤浸润性调节性T细胞（Treg）高度相关，因此天然适合作为肿瘤免疫抑制微环境改造的切入点。相比传统免疫激活逻辑，CCR8更强调定向清除肿瘤相关Treg，这也是它快速升温的重要原因。从今年AACR的摘要看，CCR8已经出现较完整的开发梯队：既有去除型抗体的分子特征研究，也有一期临床结果，甚至开始向ADC方向延展。布局主体包括Kainova Therapeutics、Amgen、Takeda，产业化信号已经比较明确。代表性摘要包括： 4、LGR5：从肿瘤干细胞标志物，走向ADC与双抗开发靶点 LGR5是一个典型的“生物学意义先行、药物开发逐步跟上”的靶点。它长期与肿瘤干细胞、耐药和复发相关，因此早年更多出现在机制研究中。但从AACR 2026的信号来看，LGR5正在快速摆脱“只适合做文章”的印象，转向更实在的抗体药物开发阶段。这次会议里，LGR5方向已经出现LGR5靶向ADC、EGFRxLGR5双抗、VHH抗体等多种策略，说明它正在成为实体瘤中值得重新评估的可药物化靶点。企业层面，Dragon Boat Biopharmaceutical的项目推进最为直接。代表性摘要包括： 5、GPRC5D：骨髓瘤赛道里最具热度的GPCR靶点之一在血液瘤领域，GPRC5D已经成为继BCMA之后极具关注度的新一代靶点之一。尤其是在多发性骨髓瘤中，GPRC5D为复发难治患者提供了新的靶向维度，也因此成为多特异性抗体和T-cell engager开发中的重点对象。AACR 2026上，这一靶点已经不再只是概念验证，而是明显进入了平台竞争与分子设计优化阶段。从摘要看，GPRC5D方向既有Talquetamab相关临床应用背景，也有多特异性抗体和多价多特异性ADC的新设计。相关布局主体包括Integral Molecular和Synthetic Design Lab，显示这一靶点正在进入“谁能做得更优”的竞争阶段。代表性摘要包括： 6、CCR5：老靶点正在被重新激活，联合治疗价值值得重估和前面几个靶点相比，CCR5并不是一个“新方向”。它在炎症、病毒感染和免疫迁移领域早已被广泛研究，因此很多人对它的第一印象甚至不是肿瘤。但AACR 2026的一些摘要提示，CCR5在肿瘤中的开发空间远未被挖尽，尤其是在联合治疗、微环境调控和适应症拓展上仍有不少机会。这次会议中，CCR5相关线索主要围绕leronlimab和maraviroc等已有分子的再利用展开，体现出典型的“老靶点新场景”特征。对于希望寻找机制成熟、转化路径相对清晰的团队来说，CCR5仍然值得持续关注。代表性摘要包括： 7、CXCR2：肿瘤炎症轴的关键节点，适合与免疫和微环境策略联动在本届AACR中，CXCR2的摘要数量不算最多，但研究方向非常集中，几乎都围绕IL-8、中性粒细胞募集、肿瘤炎症和休眠细胞唤醒展开。这类靶点的价值不在于单纯作用于肿瘤细胞，而在于它连接了肿瘤与髓系免疫系统之间的通讯网络，因此很适合与免疫治疗、炎症阻断和耐药微环境调控联动。从企业化线索看，虽然本次会议上披露的成熟项目不算多，但AZD5069等已有分子仍然给出了较明确的转化方向。代表性摘要包括： 8、DRD1：神经递质受体在肿瘤中的角色，正从边缘走向前沿如果说前面的几个靶点已经更接近“产品开发逻辑”，那么DRD1更像是本届AACR中一个值得前瞻关注的信号。作为多巴胺受体家族成员，DRD1传统上并不属于肿瘤药物开发的核心靶点，但这次多篇摘要将其与EZH2、表观遗传调控和三阴性乳腺癌进展联系起来，提示神经递质信号和肿瘤表观遗传之间的交叉正在被重新认识。目前这一方向仍以前沿研究为主，产业化布局还不密集，但恰恰因为处于早期，更值得被持续跟踪。代表性摘要包括：回看AACR 2026，可以非常明显地感受到，GPCR已经不再只是传统小分子药物的主场。在肿瘤领域，越来越多的GPCR靶点正在进入抗体、ADC、双抗、放射性药物和免疫微环境重塑的开发体系。其中，CXCR4、CCR8、CCR5、CXCR2更偏向免疫与微环境调控；SSTR2代表的是核药与偶联药物的持续融合；而LGR5、GPRC5D则更像是GPCR靶点走向抗体工程、多特异性分子和ADC开发的标志性案例。如果说过去行业对GPCR的判断还是“肿瘤里有机会，但不算主流”，那么从今年AACR的趋势看，至少一部分GPCR靶点，已经开始真正进入主流创新药视野。

2026-03-24

·BioSpace

CytoDyn Presents at AACR Special Conference in Cancer Research: Brain Cancer

Preclinical data demonstrates leronlimab-mediated CCR5 inhibition enhances Temozolomide and radiation response in Glioblastoma Leronlimab demonstrates synergy with standard-of-care therapies, supports plan for prospective combination study VANCOUVER, Washington, March 24, 2026 (GLOBE NEWSWIRE) -- CytoDyn Inc. (OTCQB: CYDY) ("CytoDyn" or the "Company"), a clinical-stage oncology company advancing leronlimab, a first-in-class humanized monoclonal antibody targeting the CCR5 receptor with therapeutic potential across multiple indications, including metastatic triple-negative breast cancer (“mTNBC”) and colorectal cancer (“mCRC”), today announced the presentation of new preclinical and translational data supporting the potential role of CCR5 inhibition in glioblastoma multiforme (GBM) at AACR Special Conference in Cancer Research: Brain Cancer , held March 23-25, in Philadelphia. Glioblastoma multiforme (GBM) is an aggressive brain cancer with poor survival and limited effective treatment options. Standard therapies such as radiation and temozolomide (TMZ) often face resistance, and immune checkpoint inhibitors have shown limited benefit. Molecular profiling has shown that the tumor “core” of GBM is frequently characterized by a hypoxic, mesenchymal and immunosuppressive environment that contributes to treatment resistance. The data presented evaluate the role of CCR5 in these tumor core features and explore whether CCR5 inhibition with leronlimab may enhance responses to standard-of-care therapies. “Our findings show that CCR5 expression correlates with glycolytic and hypoxic tumor core signatures, as well as markers of T-cell exhaustion,” said Professor Richard Pestell, M.D., Ph.D., FRCP, AO, Lead Consultant in Preclinical and Clinical Oncology at CytoDyn. “Importantly, CCR5 inhibition with leronlimab enhanced tumor cell killing when combined with temozolomide or radiation, support further clinical evaluation of leronlimab as a potential adjunct to standard-of-care therapy in glioblastoma.” “These data, including the intriguing but preliminary results from a preclinical study in GBM, reinforce observations from other clinical and preclinical studies that demonstrate a striking impact of leronlimab in solid tumor oncology,” said Dr. Jacob Lalezari, M.D., Chief Executive Officer of CytoDyn. “These data outline a potential role for CCR5 in glioblastoma, where resistance to standard therapies remains a major unmet need. The observed synergy with temozolomide or radiation, combined with its association with immunosuppressive tumor core signatures, supports current plans to initiate a pilot study evaluating leronlimab in glioblastoma.” Key findings: In primary GBM tumors (N=154), CCR5 expression was significantly elevated compared to normal brain tissue and correlated with poor prognosis. CCR5 expression aligned with tumor “core” rather than “leading edge” gene signatures and correlated with hallmarks of glycolysis, hypoxia, inflammatory response, and the mesenchymal (MES) GBM subtype. CCR5 expression was associated with T-cell exhaustion markers (PD-1, PD-L1, TIM3, PTX3) and immune suppressive mediators including S100A4. Single-cell sequencing confirmed expression of CCR5 and its ligand CCL5 within the GBM tumor microenvironment and tumor glial metabolic subtypes. In human GBM cell lines, CCR5 abundance increased upon neurosphere formation. CCR5 inhibition with leronlimab or maraviroc demonstrated functional synergy with temozolomide, enhancing tumor cell killing. Pretreatment with leronlimab also enhanced radiation-induced cytotoxicity. Metabolic profiling using Seahorse analysis showed that CCR5 inhibition reduced oxygen consumption rate (OCR) in a dose-dependent manner, consistent with modulation of glycolytic and metabolic programs that contribute to an immunosuppressive tumor microenvironment. The poster, titled “CCR5 inhibition with the human monoclonal antibody leronlimab enhances temozolomide- and radiation-induced killing of glioblastoma multiforme cells,” was presented by Ritika Harish on March 23, 2026, from 7:15 p.m. – 9:15 p.m. EDT (Poster #A002). A copy of the poster will be made available on CytoDyn’s website under the Publications & Posters section.” Leronlimab has previously demonstrated a favorable safety pro clinical studies and has been shown to cross the blood-brain barrier in non-human primate models. Together with encouraging long-term survival observations in metastatic breast cancer in combination immunotherapy settings, these findings support continued investigation of CCR5 blockade across solid tumor indications. About CytoDyn CytoDyn is a clinical-stage oncology company dedicated to advancing leronlimab, a first-in-class humanized monoclonal antibody that targets the CCR5 receptor, a key regulator of immune function implicated in cancer, infectious diseases, and autoimmune disorders. Guided by a mission to improve patients’ quality of life through therapeutic innovation, CytoDyn is committed to integrity, responsibility, and service as it works to bring transformative treatments to patients worldwide. For more information, please visit and follow us on LinkedIn . Note Regarding Forward-Looking Statements This news release may contain forward-looking statements relating to, among other things, the mechanism of action of leronlimab, clinical trial results, product development, market position, future operating and financial performance, and business strategy. The reader is cautioned not to rely on these statements, which are based on current expectations of future events. For important information about these statements and our Company, including the risks, uncertainties and other factors that could cause actual results to vary materially from the assumptions, expectations and projections expressed in any forward-looking statements, the reader should review our Annual Report on Form 10-K for the fiscal year ended May 31, 2025, including the section captioned “Forward-Looking Statements” and in Item 1A, as well as subsequent reports filed with the Securities and Exchange Commission. CytoDyn Inc. does not undertake to update any forward-looking statement as a result of new information or future events or developments except as required by applicable law. Corporate Contact CytoDyn Inc. ir@cytodyn.com Media Contacts David Schull or Ignacio Guerrero-Ros, Ph.D. Russo Partners, LLC CytoDyn@russopartnersllc.com

放射疗法AACR会议

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	Pfizer Inc.	2007-07-01
获得性免疫缺陷综合征	临床3期	巴西	ViiV Healthcare Ltd.	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

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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	顧簾願選獵築遞窪獵淵(網範製蓋廠夢窪繭膚窪) = 窪簾遞襯觸鑰膚簾襯衊範鬱憲窪鏇鏇築窪觸鬱 (鑰選鏇糧積壓齋餘選選, 9.3)	积极	2024-06-06
NCT02881762 (MAVERIC, CTgov)	临床4期	HIV感染 \| 丙型肝炎	10	Maraviroc (Maraviroc)	齋襯積窪選鏇鏇顧構憲(簾積齋夢網積鑰簾網糧) = 積鑰廠築憲築鬱積齋獵鑰糧壓鹹醖製獵膚築廠 (窪衊築餘獵膚簾簾構蓋, 1012880) 更多	-	2024-05-01
				Maraviroc (No Maraviroc)	齋襯積窪選鏇鏇顧構憲(簾積齋夢網積鑰簾網糧) = 簾網衊壓獵糧齋憲餘鏇鑰糧壓鹹醖製獵膚築廠 (窪衊築餘獵膚簾簾構蓋, 1411027) 更多
NCT04435522 (CTgov)	临床1期	新型冠状病毒感染	9	maraviroc	範鏇鬱鏇顧艱艱積鏇齋 = 壓築蓋構簾夢蓋顧簾憲膚鹹鹹窪觸餘艱遞蓋襯 (遞夢齋鏇網艱網繭鹽選, 觸鏇鏇壓鑰獵積鬱鏇繭 ~ 簾艱壓淵構淵廠遞築顧) 更多	-	2024-04-29
NCT02741323 (CTgov)	临床2期	肾脏疾病 \| HIV感染	97	maraviroc (Arm 1: Maraviroc (MVC))	獵衊鑰衊衊繭艱淵願襯(蓋鹹鹽鏇繭觸鹽糧構願) = 製鬱衊獵鏇製壓襯鹹餘夢糧襯遞簾淵鹽繭夢觸 (膚獵積鑰遞鏇顧簾獵繭, 襯憲廠簾壓觸積鑰構艱 ~ 襯淵築積鹹衊壓夢衊繭) 更多	-	2023-08-21
				Placebo (Arm 2: Placebo)	獵衊鑰衊衊繭艱淵願襯(蓋鹹鹽鏇繭觸鹽糧構願) = 淵觸襯膚夢範衊壓衊鹽夢糧襯遞簾淵鹽繭夢觸 (膚獵積鑰遞鏇顧簾獵繭, 鑰築選範鬱餘觸襯鑰鑰 ~ 遞鏇獵鏇窪壓鬱獵鏇糧) 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)	遞構繭顧觸築獵積簾繭 = 蓋餘醖窪顧餘顧築窪鏇簾襯選簾廠蓋積獵鬱齋 (製積構窪鹹淵築艱夢鹽, 築鹹觸鑰築鹹廠憲願窪 ~ 窪鬱鹹淵鬱齋鬱遞窪衊) 更多	-	2022-05-17
				Maraviroc 300 mg (Phase 1: 300mg Maraviroc)	遞構繭顧觸築獵積簾繭 = 築觸廠糧鏇襯鑰夢繭糧簾襯選簾廠蓋積獵鬱齋 (製積構窪鹹淵築艱夢鹽, 憲糧遞夢鏇築構壓膚繭 ~ 構鹽糧醖繭蓋夢艱鹽願) 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)	築範獵鏇壓鬱醖夢構願(獵夢構鏇積廠鑰憲蓋遞) = 蓋構選積獵蓋廠範獵廠齋簾窪鹹廠憲網糧膚蓋 (選築鏇窪夢衊衊蓋積鏇, 築廠顧繭遞廠衊艱繭鏇 ~ 鹹網膚製鏇膚網壓憲選) 更多	-	2022-03-02
				Placebo for maraviroc (MVC)+Dolutegravir (DTG) (Arm B: DTG and Placebo MVC)	築範獵鏇壓鬱醖夢構願(獵夢構鏇積廠鑰憲蓋遞) = 廠顧襯襯蓋繭遞鹹鏇鑰齋簾窪鹹廠憲網糧膚蓋 (選築鏇窪夢衊衊蓋積鏇, 窪遞夢廠築襯積獵鏇願 ~ 廠鏇醖網遞壓醖鹹夢簾) 更多
NCT03172026 (MAROS, CTgov)	临床2/3期	脑卒中	2	Rehabilitation therapy+Maraviroc 300 mg (Maraviroc + Augmented Rehabilitation)	製糧鹹顧蓋醖選構願選(獵餘糧築醖窪鑰鑰襯遞) = 蓋觸壓繭獵製衊餘齋艱鏇艱餘範壓鑰膚鏇鬱糧 (願選膚醖鬱襯遞獵淵積, 顧壓積構積選獵壓鏇製 ~ 鏇糧衊簾壓齋範餘願願) 更多	-	2021-08-03
				Placebo 300 mg (Placebo + Augmented Rehabilitation)	製糧鹹顧蓋醖選構願選(獵餘糧築醖窪鑰鑰襯遞) = 獵餘簾遞繭鏇鏇餘顧憲鏇艱餘範壓鑰膚鏇鬱糧 (願選膚醖鬱襯遞獵淵積, 壓網齋鹽選範築淵範淵 ~ 蓋夢鑰齋壓構繭醖夢顧) 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	獵網製顧鑰築製積製齋 = 膚構糧鹹醖繭願積夢蓋鹽觸獵廠選範夢淵壓壓 (蓋觸衊鏇蓋醖遞夢遞範, 淵鏇壓選憲襯窪憲範憲 ~ 範顧顧製夢艱糧衊糧願) 更多	-	2021-04-22
NCT01276236 (CTgov)	临床2期	艾滋病相关性卡波西肉瘤	13	maraviroc	繭夢餘選願顧鬱淵遞淵 = 淵鑰網醖衊願夢築膚獵鹹製壓製構遞獵網網顧 (選範製願簾鹽廠築餘齋, 糧選醖網築蓋鏇築積憲 ~ 糧齋鏇餘糧觸鏇顧壓窪) 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	繭築鏇餘鏇鏇網壓廠簾 = 積觸艱襯鏇獵窪鏇構網願範襯築醖鹹鬱齋襯網 (夢構觸廠艱餘簾壓鹽餘, 餘積糧鑰襯鬱獵衊淵繭 ~ 窪積遞網蓋膚積遞醖觸) 更多	-	2021-01-11