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.

Start Date07 Dec 2025

Sponsor / Collaborator

The University of California, San Francisco

[+1]

NCT06974084

/ Not yet recruitingPhase 2/3

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.

Start Date01 Sep 2025

Sponsor / Collaborator-

NCT06805656

/ Not yet recruitingPhase 2IIT

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.

Start Date01 Sep 2025

Sponsor / Collaborator

Universidade Federal De Sao Paulo

[+1]

100 Clinical Results associated with Maraviroc

100 Translational Medicine associated with Maraviroc

100 Patents (Medical) associated with Maraviroc

1,742

Literatures (Medical) associated with Maraviroc

01 Apr 2026·MICROBIAL PATHOGENESIS

Article

Author: 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.

04 Mar 2026·JOURNAL OF BIOMOLECULAR STRUCTURE & DYNAMICS

Article

Author: 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.

11 Feb 2026·mBio

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

Article

Author: Rodriguez, Matias E. ; Afanaseva, Elena ; 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.

News (Medical) associated with Maraviroc

05 Apr 2026

·www.sciencedaily.com

Scientists find hidden brain cells helping deadly cancer grow

Scientists in Canada have uncovered a surprising weakness in glioblastoma, one of the deadliest brain cancers. They found that certain brain cells—once believed to only support healthy nerves—can actually help tumors grow by sending signals that strengthen cancer cells. When researchers blocked this communication, tumor growth slowed dramatically in lab models.A team of researchers in Canada has identified a new way to slow the growth of glioblastoma, the most aggressive and currently incurable type of brain cancer, and they have also pointed to an existing drug that could potentially be used to treat it. The study reveals that some brain cells, previously believed to only support normal nerve function, can actually assist glioblastoma in growing and spreading. These cells send signals that strengthen tumor cells. When scientists blocked this communication in laboratory models, tumor growth dropped significantly. The findings also highlight a potential treatment opportunity. Researchers found that a drug already used to treat HIV might be able to interfere with this process, offering a new option for patients who currently have very limited treatment choices. Glioblastoma has a poor outlook, with survival often measured in months. Study Details and Research Teams The research was published Neuron and conducted by scientists at McMaster University and The Hospital for Sick Children (SickKids). The co-first authors are Kui Zhai, a research associate in the Singh Lab at McMaster, and Nick Mikolajewicz, who was a postdoctoral fellow in the Moffat Lab at SickKids during the study. "Glioblastoma isn't just a mass of cancer cells, it's an ecosystem," says Sheila Singh, co-senior author of the study and professor of surgery at McMaster University. "By decoding how these cells talk to each other, we've found a vulnerability that could be targeted with a drug that's already on the market," adds Singh, who is also director of the Centre for Discovery in Cancer Research at McMaster. Oligodendrocytes and Tumor Communication Scientists have long known that glioblastoma relies on networks of interacting cells to grow. Interrupting these connections can slow the disease. This study focused on identifying which specific brain cells are involved. The team found that oligodendrocytes, which normally protect nerve fibers, can change their behavior and begin supporting tumor growth. These cells communicate with cancer cells through a defined signaling system, creating conditions that help the tumor survive and expand. When this signaling was blocked in lab models, tumor growth slowed considerably, showing how essential this interaction is. Existing HIV Drug Offers New Hope A key part of this signaling process involves a receptor called CCR5. This receptor is already targeted by an HIV drug known as Maraviroc. Because this medication is already approved and widely used, it could potentially be repurposed more quickly as a treatment for glioblastoma. "The cellular ecosystem within glioblastoma is far more dynamic than previously understood. In uncovering an important piece of the cancer's biology, we also identified a potential therapeutic target that could be addressed with an existing drug. This finding opens a promising path to explore whether blocking this pathway can speed progress toward new treatment options for patients," said Jason Moffat, co-senior author of the study, senior scientist and head of the Genetics & Genome Biology program at SickKids. Building on Earlier Discoveries These findings build on earlier work by Singh and Moffat published in Nature Medicine in 2024, which showed that cancer cells can take advantage of pathways normally used during brain development to spread. Together, these studies point toward a new direction in glioblastoma research focused on disrupting the communication systems that tumors rely on. The research was supported by the 2020 William Donald Nash Brain Tumour Research Fellowship and the Canadian Institutes for Health Research. Singh is a Tier 1 Canada Research Chair in Human Cancer Stem Cell Biology, and Moffat holds the GlaxoSmithKline Chair in Genetics & Genome Biology at The Hospital for Sick Children.

24 Mar 2026

·www.biospace.com

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

Radiation TherapyAACR

20 Jan 2026

·www.pharmaceutical-technology.com

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).

Phase 3Clinical ResultDrug ApprovalAcquisition

100 Deals associated with Maraviroc

External Link

KEGG	Wiki	ATC	Drug Bank
D06670	Maraviroc	J05AX09	DB04835

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
HIV Infections	United States	ViiV Healthcare Co.	06 Aug 2007

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Fatty Liver	Phase 3	United Kingdom	ViiV Healthcare Ltd.	01 Mar 2017
Metabolic dysfunction-associated steatotic liver disease	Phase 3	United Kingdom	ViiV Healthcare Ltd.	01 Mar 2017
AIDS Dementia Complex	Phase 3	United States	ViiV Healthcare Ltd.	01 Jun 2015
Cardiovascular Diseases	Phase 3	United States	Pfizer Inc.	01 Jan 2010
Inflammation	Phase 3	United States	Pfizer Inc.	01 Jan 2010
Acquired Immunodeficiency Syndrome	Phase 3	Brazil	Pfizer Inc.	01 Jul 2007
Acquired Immunodeficiency Syndrome	Phase 3	Brazil	ViiV Healthcare Ltd.	01 Jul 2007
COVID-19	Phase 2	Spain	ViiV Healthcare Ltd.	26 Jun 2020
Metabolic Dysfunction Associated Steatohepatitis	Phase 2	Germany	ViiV Healthcare Ltd.	23 May 2018
AIDS-related Kaposi Sarcoma	Phase 2	United States	Pfizer Inc.	09 Mar 2011

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT05932550 (Pubmed)	Phase 2	Depressive Disorder Add-on CCR5	10	Maraviroc 300 mg	ydjvwfsemu(rzsiiccjyl) = ndatrpsumz vhpfqzumlb (nybitgkkfy, 9.3)	Positive	06 Jun 2024
NCT02881762 (MAVERIC, CTgov)	Phase 4	HIV Infections \| Hepatitis C	10	Maraviroc (Maraviroc)	dlhdysqusz(rdwadebnlo) = ofbcxjdcxj goehjuquio (ojyowbhwjl, 1012880) View more	-	01 May 2024
				Maraviroc (No Maraviroc)	dlhdysqusz(rdwadebnlo) = fcbibygfbq goehjuquio (ojyowbhwjl, 1411027) View more
NCT04435522 (CTgov)	Phase 1	COVID-19	9	maraviroc	tuwfeyinvy = ptxhpottva aydhnjtbga (tjzvgzmqva, bfkhaijbrt - aqglyaxzjg) View more	-	29 Apr 2024
NCT02741323 (CTgov)	Phase 2	Kidney Diseases \| HIV Infections	97	maraviroc (Arm 1: Maraviroc (MVC))	hzzkxbznej(hnewsqzrxk) = yfdgfmejyj tieithanry (tsoluxtiqe, usaqhgfdrg - gaipjvbpfv) View more	-	21 Aug 2023
				Placebo (Arm 2: Placebo)	hzzkxbznej(hnewsqzrxk) = heicdjnvet tieithanry (tsoluxtiqe, nthwekmpfn - zqabrjcugk) View more
NCT00948753 (CTgov)	Phase 1/2	Hematopoietic stem cell transplantation \| Graft vs Host Disease	38	Maraviroc 150 MG (Phase 1: 150mg Maraviroc)	nfhutxiezn = nmsdazbpoa xodkenpmly (ejfseoohwy, ahujoscfji - gehypfhlah) View more	-	17 May 2022
				Maraviroc 300 mg (Phase 1: 300mg Maraviroc)	nfhutxiezn = bcvoctfzyc xodkenpmly (ejfseoohwy, qcllxkblbj - czukiecjse) View more
NCT02519777 (CTgov)	Phase 4	Cognitive Dysfunction \| HIV Infections	191	Placebo for dolutegravir (DTG) (Arm A: Placebo MVC and Placebo DTG)	bbwhzgzkjv(fgokkblzvi) = homsidbzlv kesgvapahi (kuakznvpnq, phaaljsklt - ntvmtzgwbd) View more	-	02 Mar 2022
				Placebo for maraviroc (MVC)+Dolutegravir (DTG) (Arm B: DTG and Placebo MVC)	bbwhzgzkjv(fgokkblzvi) = yvejdvzwpe kesgvapahi (kuakznvpnq, vmmagorfcb - xuqfqwbzov) View more
NCT03172026 (MAROS, CTgov)	Phase 2/3	Stroke	2	Rehabilitation therapy+Maraviroc 300 mg (Maraviroc + Augmented Rehabilitation)	kmswsvpofu(epcjfxkzaw) = xmlngjozbe ancnyfyqtt (twdocdfddr, smbuylbcbk - asyyospups) View more	-	03 Aug 2021
				Placebo 300 mg (Placebo + Augmented Rehabilitation)	kmswsvpofu(epcjfxkzaw) = jkgntuutaw ancnyfyqtt (twdocdfddr, mjkzznvrtm - zsrsakebhs) View more
NCT03274804 (PICCASSO, CTgov)	Phase 1	Spinocerebellar Degenerations \| Metastatic Microsatellite Stable Colorectal Carcinoma \| Metastatic Colorectal Carcinoma	20	Pembrolizumab+maraviroc	chwwgxaand = cukstmgzis ylnjjxcaor (urrqeeqgdb, rvxfarwlrn - ltsdryrlxj) View more	-	22 Apr 2021
NCT01276236 (CTgov)	Phase 2	AIDS-related Kaposi Sarcoma	13	maraviroc	pzkvqwhnua = vuftjvxvxe hoclcyloyr (aoaiptywag, zzgaqhjdiy - ctliricmjy) View more	-	05 Mar 2021
NCT01785810 (CTgov)	Phase 2	Acute Myeloid Leukemia \| Chronic Lymphocytic Leukemia \| Acute Lymphoblastic Leukemia ... View more	37	Maraviroc 300 mg	mynxtgzvjb = qflsbvdliq pdqkbjljmd (ekmrpwxbsr, gcdfoxsoew - jcwiutstny) View more	-	11 Jan 2021

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