RegulationOrphan Drug (United States), Orphan Drug (European Union), Conditional marketing approval (China), Orphan Drug (Japan), Orphan Drug (South Korea)

Structure/Sequence

Molecular FormulaC28H54N8

InChIKeyYIQPUIGJQJDJOS-UHFFFAOYSA-N

CAS Registry110078-46-1

179

Clinical Trials associated with Plerixafor

NCT07605416

/ Not yet recruitingPhase 2IIT

Quadruplet Induction Followed by Teclistamab Consolidation and Doublet Maintenance in Patients With Primary Plasma Cell Leukemia: The QUANTUM Trial

This phase II trial compares standard consolidation with daratumumab, carfilzomib, lenalidomide, and dexamethasone to consolidation with teclistamab following standard induction therapy and autologous hematopoietic stem cell transplant for improving overall survival of patients with plasma cell leukemia. Consolidation therapy is treatment given after initial therapy to kill any cancer cells that may remain in the body. Daratumumab is in a class of medications called monoclonal antibodies. It binds to a protein called CD38, which is found on some types of immune cells and cancer cells, including myeloma cells. Daratumumab may block CD38 and help the immune system kill cancer cells. Carfilzomib inhibits protein complexes called proteasomes, which inhibits cancer cell growth and leads to cancer cell death. Lenalidomide may help kill cancer cells and prevents the growth of blood vessels that cancer cells need to survive. Dexamethasone is in a class of medications called corticosteroids. It is used to reduce inflammation and lower the body's immune response to help lessen the side effects of chemotherapy drugs. Teclistamab is a monoclonal antibody that may interfere with the ability of cancer cells to grow and spread. A monoclonal antibody is a type of protein that can bind to certain targets in the body, such as molecules that cause the body to make an immune response (antigens). Giving teclistamab as consolidation therapy after induction and autologous hematopoietic stem cell transplant may improve survival outcomes in patients with plasma cell leukemia, compared to standard consolidation with daratumumab, carfilzomib, lenalidomide, and dexamethasone.

Start Date01 Jul 2026

Sponsor / Collaborator

National Cancer Institute

NCT07585136

/ Not yet recruitingPhase 1IIT

Stem Cell Mobilization and Apheresis for Life-threatening Blood Disorders

The purpose of this study is to investigate mobilization and collection of HSPCs in patients with bone marrow failure syndromes (BMFS) using granulocyte-colony stimulating factor (otherwise known as Filgrastim) with plerixafor to demonstrate safety and feasibility of collecting HSPCs to advance gene therapy.
Primary objective:
- To characterize the safety of Filgrastim plus plerixafor in participants with bone marrow failure syndromes as determined by the incidence of adverse events (AEs).
Secondary Objectives:
* To characterize the feasibility of HSPC mobilization using Filgrastim plus plerixafor as determined by peripheral blood CD34+ counts.
* To measure the mobilization effects of Filgrastim plus plerixafor in the peripheral blood in participants as determined by peak peripheral blood CD34+ counts.
* To estimate efficacy of Filgrastim plus plerixafor for HSPC mobilization and apheresis collection in participants as determined by the yield of CD34+ cells (CD34+ cells/kg).

Start Date01 Jun 2026

Sponsor / Collaborator

St. Jude Children's Research Hospital, Inc.

NCT07341022

/ Not yet recruitingPhase 1/2IIT

HEMATOPOIETIC STEM CELL MOBILIZATION USING HIGH-DOSE PLERIXAFOR IN PATIENTS WITH SICKLE CELL DISEASE: A CONTROLLED PHASE I/II TRIAL.

The objective of this study is to demonstrate whether high-dose plerixafor can effectively mobilize hematopoietic stem cells in patients with sickle cell disease. It will also learn about the safety of this drug in higher doses in these patients. The main questions it aims to answer are:
Does high-dose plerixafor mobilize enough hematopoietic stem cells? What medical problems do participants have when taking high-dose plerixafor?
Participants will:
Undergo transfusion Take high-dose plerixafor Be submitted to stem cell collection by apheresis Visit the clinic 10 days after the procedure Be contacted by the research team 30 days after the procedure.

Start Date01 Jun 2026

Sponsor / Collaborator

Hospital Israelita Albert Einstein

[+1]

100 Clinical Results associated with Plerixafor

100 Translational Medicine associated with Plerixafor

100 Patents (Medical) associated with Plerixafor

2,325

Literatures (Medical) associated with Plerixafor

01 Jul 2026·INTERNATIONAL IMMUNOPHARMACOLOGY

Berberine pretreatment enhances the homing and anti-inflammatory efficacy of dental pulp mesenchymal stem cells in TNBS-induced inflammatory bowel disease via activating the CXCR4/SDF-1 signaling pathway

Article

Author: Peng, Bo ; Qian, Xin ; Wu, Chenchen ; Zheng, Jiawen ; Zou, Xiaoping ; Zhou, Fan

OBJECTIVE:

Inflammatory bowel disease (IBD) is a chronic intestinal disorder characterized by immune dysregulation and persistent inflammation. Mesenchymal stem cell (MSC) therapy shows promise but is limited by low homing efficiency. This study aimed to investigate whether berberine (BBR) pretreatment enhances the homing capacity and therapeutic efficacy of dental pulp MSCs (DP-MSCs) in IBD, and to clarify the role of the CXCR4/SDF-1 signaling pathway in immunomodulation.

METHODS:

Human dental pulp mesenchymal stem cells were isolated and identified. Through in vitro screening experiments (berberine, curcumin, quercetin, and liquiritigenin), 2 μmol/L BBR was determined to be the optimal pretreatment concentration (verified by CCK-8 and apoptosis experiments).A TNBS-induced mouse IBD model was established,and mice were randomized into Control,TNBS,TNBS+DP-MSC,TNBS+BBR-pretreated DP-MSC(BBR-DPMSC) groups,the DP-MSC + AMD3100 group, and the BBR-DPMSC+AMD3100 group.(n = 6/group). DP-MSCs or BBR-DPMSCs were administered via tail vein injection.AMD3100(CXCR4 pathway blocker) was administered by intraperitoneal injection.The intestinal inflammation and immune regulatory effects were evaluated by colon length measurement, disease activity index (DAI) score, HE staining and pathological score, and ELISA (IL-1β,IL-6,IL-10,TGF-β,SDF-1,CXCR4). In vivo live imaging assessed DP-MSC homing. Transwell assays and CXCR4 inhibitor AMD3100 were used to verify the CXCR4/SDF-1 pathway.

RESULTS:

In vitro screening demonstrated that berberine had the best pro-proliferative and anti-apoptotic effects on DP-MSCs among the four natural compounds (P < 0.01). In the IBD mouse model, compared with the untreated DP-MSCs, BBR-DPMSCs alleviated colonic shortening, reduced DAI scores, decreased intestinal mucosal damage and inflammatory cell infiltration, and regulated cytokine levels: lowering serum IL-1β and IL-6, and increasing anti-inflammatory factors IL-10 and TGF-β.Live imaging demonstrated that berberine significantly enhanced the homing efficiency of DP-MSCs to the injured intestine. In the TNBS model, SDF-1 was mainly highly expressed in the intestinal tissue, forming a specific chemotactic gradient. Transwell experiments confirmed that berberine promoted the migration of DP-MSCs in an SDF-1 concentration-dependent manner. Meanwhile, BBR could up-regulate the expression of CXCR4 in DP-MSCs. After blocking the CXCR4/SDF-1 pathway with AMD3100, the homing enhancement effect and therapeutic effect of the BBR-DP-MSC group were significantly decreased.

CONCLUSION:

BBR pretreatment enhances the intestinal homing capacity of DP-MSCs via activating the CXCR4/SDF-1 signaling pathway, and exerts synergistic anti-inflammatory effects by upregulating IL-10 and TGF-β secretion, ultimately improving the therapeutic efficacy in IBD. This study provides a novel strategy for optimizing MSC-based immunotherapy of IBD by combining natural compounds with stem cells.

01 Jul 2026·Hematology Transfusion and Cell Therapy

Derived hematological indices during peripheral blood stem cell mobilization in the plerixafor era: insightful dynamics but limited predictive value

Article

Author: Sindhu, Edakkadath Raghavan ; Niveditha, Lakshmi P ; Murugesan, Mohandoss ; Nair, Chandran K

INTRODUCTION:

Derived hematological indices reflect immune activation, but their dynamics during the plerixafor era and their predictive value for stem cell yield remain unclear.

OBJECTIVES:

To assess changes in derived hematological inflammatory markers during peripheral blood stem cell mobilization in autologous patients and allogeneic donors, and to evaluate their correlation with CD34⁺ stem cell yield. These markers include ratios (neutrophil-to-lymphocyte, platelet-to-lymphocyte and lymphocyte-to-monocyte), and composite indices (systemic immune-inflammation and systemic inflammation response indices).

METHODS:

A retrospective analysis was conducted of 127 autologous and 53 allogeneic mobilization events between January 2019 and March 2024. Blood counts and derived indices were analyzed before and after granulocyte colony-stimulating factor administration with and without plerixafor. CD34⁺ cell enumeration was performed after mobilization. Dynamic changes in inflammatory indices and their correlation with CD34⁺ counts were assessed.

RESULTS:

After mobilization, there was a significant increase in the neutrophil-to-lymphocyte ratio, systemic immune-inflammation index, and systemic inflammation response index, and a decrease in the platelet-to-lymphocyte and lymphocyte-to-monocyte ratios in both groups. While allogeneic donors had higher CD34⁺ counts (median 110 cells/µL versus 48 cells/µL in autologous), no consistent correlation was found between dynamic inflammatory marker changes and CD34⁺ yield. Plerixafor use in autologous patients significantly influenced the platelet-to-lymphocyte ratio and systemic immune-inflammation index dynamics, highlighting its role in modulating the acute inflammatory response in the plerixafor era.

CONCLUSIONS:

Inflammatory markers change significantly during mobilization with granulocyte colony-stimulating factor, reflecting acute immune activation. However, the studied markers do not predict CD34⁺ yield and should not replace direct enumeration. Their role may be better suited to complement biological understanding rather than clinical decision-making.

01 Jun 2026·INTERNATIONAL IMMUNOPHARMACOLOGY

Intermittent fasting attenuates ovarian chronic inflammation in obese mice by inhibiting the CXCL12–CXCR4 axis

Article

Author: Yu, Xiaolong ; Han, Ziyun ; Chen, Xiao ; Hao, Xiaoqiong

AIM:

Obesity disrupts ovarian function in female via chronic inflammation. Intermittent fasting (IF) prevents obesity and exerts protective effects against inflammation. However, the underlying mechanisms remain poorly understood. This study aimed to elucidate the effects and putative mechanisms of action of IF on obesity-induced ovarian dysfunction.

METHODS:

Ovarian samples were collected from mice fed a normal diet (ND), high-fat diet (HFD), HFD + IF, ND + AMD3100, and HFD + AMD3100. Ovarian function was evaluated using HE staining, ELISA, TUNEL assay, and Ki67 staining. Mitochondrial function in oocytes and granulosa cells was assessed using TEM and western blotting. ROS levels were determined by dihydroethidium staining. Macrophage activation and immune cell infiltration in ovarian tissue were analyzed using immunofluorescence and flow cytometry. Transcriptomic analysis, qPCR, and western blotting were performed to delineate the regulatory networks underlying the effects of IF.

RESULTS:

HFD-induced obesity triggered ovarian chronic inflammation and various ovarian dysfunctions, including depleted follicular reserves, dysregulated hormone levels, disrupted estrous cycles, abnormal mitochondrial morphology, exacerbated oxidative stress, and increased apoptosis of granulosa cells. Importantly, IF intervention significantly alleviated chronic inflammation and reversed ovarian impairment. Mechanistically, IF suppressed the CXCL12-CXCR4 signaling axis in the ovaries of obese mice, thereby reducing the recruitment of peripheral neutrophils and inhibiting the activation of proinflammatory resident macrophages, which collectively contributed to the resolution of chronic inflammation. Inhibition of CXCR4 by AMD3100 exerted significant protective effects, effectively mitigating ovarian inflammation and preserving ovarian function in HFD-fed mice.

CONCLUSION:

Our results revealed that IF alleviated ovarian chronic inflammation in obese mice by inhibiting the CXCL12-CXCR4 axis, thereby preserving ovarian function. These findings suggest that IF and pharmacological CXCR4 blockade are potential strategies for mitigating obesity-associated female reproductive dysfunction.

News (Medical) associated with Plerixafor

30 Apr 2026

·allsci.com

European Commission approves Norgine’s Xolremdi for WHIM syndrome treatment in EU

Norgine announced that the European Commission has granted marketing authorization for Xolremdi (mavorixafor) for WHIM syndrome, making it the first therapy authorized for this condition in the European Union. The authorization, which follows a positive opinion from the European Medicines Agency’s Committee for Medicinal Products for Human Use, was granted under exceptional circumstances given the ultra-rare nature of the disease. Norgine will lead commercialization across Europe under a licensing agreement with X4 Pharmaceuticals, the US-based company that originated and holds intellectual property rights to the molecule. Xolremdi is indicated in patients aged 12 years and older for the treatment of WHIM syndrome — an acronym for warts, hypogammaglobulinemia, infections, and myelokathexis — to increase the number of circulating mature neutrophils and lymphocytes. The condition is caused by gain-of-function mutations in the CXCR4 receptor, which impairs the release of white blood cells from bone marrow into peripheral circulation, leaving affected individuals vulnerable to recurrent and severe infections. The EC authorization was granted under exceptional circumstances, a regulatory pathway applied when applicants cannot provide comprehensive efficacy and safety data due to the rarity of a condition; additional post-authorization data will be required. The authorization is supported by results from NCT03995108, a Phase III randomized, double-blind, placebo-controlled, 52-week multicenter study that enrolled 31 patients aged 12 years and older with confirmed WHIM syndrome. The trial evaluated the efficacy and safety of mavorixafor against placebo, with results published in Blood in 2024 by Badolato and colleagues. The study met its primary endpoint, demonstrating that mavorixafor increased the duration of time that absolute neutrophil and lymphocyte counts remained above defined thresholds compared with placebo. WHIM syndrome has until now been managed primarily through off-label use of filgrastim, a recombinant granulocyte colony-stimulating factor originally developed by Amgen that raises neutrophil counts but has no effect on lymphocytes, monocytes, or the wart burden associated with the condition. Plerixafor, a subcutaneously administered CXCR4 antagonist approved for stem cell mobilization, was evaluated in a Phase III crossover trial against G-CSF in WHIM syndrome but was not advanced to regulatory submission for this indication. Mavorixafor, as an oral once-daily CXCR4 antagonist that mobilizes both neutrophils and lymphocytes, occupies a distinct position as the only therapy carrying an approved label specifically for WHIM syndrome in either the US or the EU. X4 Pharmaceuticals received US FDA approval for Xolremdi in 2024. Beyond WHIM syndrome, mavorixafor is under active Phase III investigation in congenital and acquired chronic neutropenic disorders, with trial NCT06056297 currently recruiting. This article was generated with AI assistance and reviewed and edited by the AllSci editorial team Explore more at AllSci News: https://allsci.com/news/ Your email address will not be published. Required fields are marked * Comment * Name * Email * Website

04 Feb 2026

·www.biospace.com

Ayrmid Reports Additional New Real-World Data on Motixafortide for Stem Cell Mobilization in Sickle Cell Disease and Beta-Thalassemia

Key Highlights Motixafortide effectively mobilized sufficient hematopoietic stem cells (HSCs) in patients with sickle cell disease and beta-thalassemia enabling accelerated access to gene therapies 73% (11 of 15) of patients were able to collect sufficient HSC to enable progress to gene therapy manufacturing with 5 patients receiving their gene therapy and appropriately engrafted 73% (11 of 15) of patients had previously failed to collect sufficient cells with plerixafor Results support the use of motixafortide as an effective single-agent mobilizer of HSC for people with sickle cell disease and in combination with G-CSF for beta-thalassemia Findings presented at TANDEM 2026 DUBLIN, IE / ACCESS Newswire / February 4, 2026 / Ayrmid, Ltd. ("Ayrmid" or the "Company"), the parent company of Gamida Cell Inc., today announced further encouraging real-world data on the use of motixafortide, a long-acting CXCR4 inhibitor licensed by Ayrmid under the brand name APHEXDA ® , for mobilizing HSCs in patients with sickle cell disease undergoing gene therapy. The results were presented at the 2025 Transplantation & Cellular Therapy meetings of ASTCT ® and CIBMTR ® (TANDEM), taking place from February 4-7, 2026 in Salt Lake City, UT. Motixafortide is currently FDA approved in combination with filgrastim (G-CSF) for stem cell mobilization in multiple myeloma. The product's effectiveness and pharmacologic pro prompted growing interest in its potential use for sickle cell disease, where collecting adequate stem cells remains a significant barrier to gene therapy. Many patients do not mobilize enough cells with standard approaches, limiting access to curative treatment. Researchers from five treatment centers evaluated the real-world use of motixafortide in 15 patients aged 14-50. Each patient underwent one or more collection cycles over two or more days to obtain the number of stem cells required for gene therapy manufacturing. Motixafortide effectively mobilized 11 patients who had previously failed plerixafor, 3 patients mobilized effectively with motixafortide used as first line mobilization therapy. In 11 patients, sufficient cells were achieved to manufacture gene therapy for both sickle cell disease and beta-thalassemia. 5 patients have received their gene therapy and have appropriately engrafted, manufacturing is underway in a further 5 patients. Patients received Casgevy and Lyfgenia, and manufacturing is underway for Casgevy, Lyfgenia and Zynteglo. This data supports that motixafortide mobilized cells can be used across different gene therapy manufacturing platforms. Dr. John Manis,Director Transfusion Medicine Service, Associate Professor of Pathology, Harvard Medical School, commented: "The approval of gene therapies for sickle cell disease has opened the door to transformative outcomes, but inadequate stem cell collection has significantly delayed manufacturing and prevented some patients from starting treatment. These findings suggest that motixafortide may help overcome this challenge, and with more studies, expand access to potentially life-changing therapies." About Sickle Cell Disease Sickle cell disease, also known as sickle cell anemia, is a severe inherited blood disorder caused by a genetic mutation that leads to misshapen, rigid red blood cells. These cells can obstruct blood flow, causing sudden episodes of severe pain, known as pain crises, and leading to life-threatening complications. Ayrmid is dedicated to advancing therapies that help individuals living with sickle cell disease manage their symptoms and improve their quality of life. About Beta-Thalassemia Beta-thalassemia is a genetic blood disorder characterized by reduced or absent production of beta-globin, a component of hemoglobin, which is essential for carrying oxygen in red blood cells. This condition results in anemia, which can cause symptoms such as fatigue, weakness and pallor. About Ayrmid Ltd. and Gamida Cell Ayrmid Ltd. is the parent company of Gamida Cell Inc., a pioneering cell therapy company developing novel treatments designed to turn cells into powerful therapeutics. Gamida Cell Inc. currently has two FDA approved products on the market in the US, namely Omisirge ® (please see the current full Prescribing Information, including boxed warning, here ) and APHEXDA ® (please see the current full Prescribing Information here ). Gamida Cell operates as a wholly owned subsidiary of Ayrmid Limited, a UK entity. For additional information, please visit or follow Gamida Cell on LinkedIn , X , Facebook or Instagram . Contacts: Media, Investors / Business Development: bd@ayrmid.com This information is provided by RNS, the news service of the London Stock Exchange. RNS is approved by the Financial Conduct Authority to act as a Primary Information Provider in the United Kingdom. Terms and conditions relating to the use and distribution of this information may apply. For further information, please contact rns@lseg.com or visit . SOURCE: Ayrmid Pharma Ltd View the original press release on ACCESS Newswire

Gene TherapyDrug ApprovalCell Therapy

10 Dec 2025

·www.prnewswire.com

Fondazione Telethon Announces FDA approval of Waskyra™ (etuvetidigene autotemcel), a Gene Therapy for the Treatment of Wiskott-Aldrich Syndrome

WAS affects almost exclusively males, with an estimated incidence of 1 in 250,000 live male births. The therapy represents a major scientific and clinical achievement, offering new hope for patients affected by this condition. ROME, Dec. 10, 2025 /PRNewswire/ -- Fondazione Telethon announced today that the U.S. Food and Drug Administration (FDA) has approved the Biologics License Application (BLA) for Waskyra, an ex vivo gene therapy for patients with Wiskott-Aldrich syndrome (WAS), a rare and life-threatening immunodeficiency. WAS, seen almost exclusively in males, affects blood cells and cells of the immune system (the body's natural defenses). It is caused by abnormalities in the gene that produces the WAS protein found in blood cells and certain immune cells. Because people with the condition lack a functional WAS protein, their immune cells and blood cells do not develop and function normally. The FDA's approval of the BLA of Waskyra follows a positive opinion from the European Medicines Agency's Committee for Medicinal Products for Human Use for the same product just a few weeks earlier. Developed through decades of research at the San Raffaele Telethon Institute for Gene Therapy (SR-Tiget) in Milan, Waskyra represents a major scientific and clinical achievement, offering new hope for patients affected by this condition. "The FDA's approval of Waskyra is an extraordinary achievement – not only for Italian research and for Fondazione Telethon, but for the global rare disease community," said Ilaria Villa, CEO of Fondazione Telethon. "It confirms the value of a patient-centered model that turns research into real treatments, especially where the market fails to act." "The approval of this gene therapy represents a decisive step forward and a tangible response to the needs of patients," commented Dr. Alessandro Aiuti, Deputy director clinical research at SR-Tiget, Chief of Pediatric Immunohematology at IRCCS Ospedale San Raffaele and Full Professor of Pediatrics at Università Vita-Salute San Raffaele. "Seeing years of scientific research and dedication translate into real therapeutic opportunities for people gives profound meaning to our work." The clinical trial phase was conducted at IRCCS Ospedale San Raffaele, a center of excellence in gene therapy for WAS and other diseases. Fondazione Telethon is the first non-profit organization to have successfully led the full pathway of an ex vivo gene therapy from laboratory research to regulatory approval, collaborating with industry partners to bring gene therapies from discovery to patients. FDA approval further recognizes Fondazione Telethon's excellence in research and strengthens its position as an international leader in rare genetic disease research and the development of advanced therapies. About Wiskott-Aldrich syndrome (WAS) Wiskott-Aldrich syndrome is a rare genetic blood disorder that causes immunodeficiency and low platelet count, resulting from mutations in the WAS gene. The disease manifests from early childhood with recurrent and persistent infections, bleeding episodes and eczema, and is associated with an increased risk of developing autoimmune diseases and lymphomas. It affects almost exclusively males, with an estimated incidence of 1 in 250,000 live male births. Current treatment options include supportive therapies aimed at managing and preventing clinical manifestations. The only potentially curative option is hematopoietic stem cell transplantation, for which a compatible donor is not always available, and which is not without risks. About Waskyra™ (etuvetidigene autotemcel) gene therapy for Wiskott-Aldrich syndrome Waskyra consists of a single administration of autologous CD34+ hematopoietic stem and progenitor cells that have been transduced with a lentiviral vector encoding the WAS gene. Once corrected, the stem cells are reinfused into the patient, who undergoes chemotherapy beforehand to prepare the bone marrow to receive them. It has been shown that Waskyra reduces the frequency of severe and moderate bleeding events and serious infections in patients with WAS compared with the period prior to treatment. In cases where transplantation from a compatible family donor is not possible, a safe and efficacious gene therapy represents a potential therapeutic option for eligible patients. Indication and Important Safety Information What is Waskyra? Waskyra is an autologous hematopoietic stem cell-based gene therapy indicated for the treatment of pediatric patients aged 6 months and older and adults with Wiskott-Aldrich Syndrome (WAS) who have a mutation in the WAS gene for whom hematopoietic stem cell transplantation (HSCT) is appropriate and no suitable human leukocyte antigen (HLA)-matched related stem cell donor is available. What is the most important information I should know about Waskyra? During the clinical trials no adverse reactions attributable to Waskyra nor to conditioning regimen were reported. Some side effects are related to pre-treatment and other study procedures. Treatment with Waskyra is preceded by medical interventions, namely haematopoietic stem cell collection through peripheral blood mobilisation with G-CSF with or without plerixafor followed by apheresis, pre-treatment with rituximab (anti-CD20 monoclonal antibody) and reduced intensity conditioning, which carry their own risks. When assessing the safety of a treatment with Waskyra, the safety profile and product information of the medicinal products used for peripheral blood mobilisation, pre-treatment and reduced intensity conditioning should be considered, in addition to the risks linked to the gene therapy. Negative side effects of prescription drugs are encouraged to report to the FDA. Visit , or call 1–800-FDA-1088. For complete product information, please see the full Prescribing Information at Site: Package Insert: About Fondazione Telethon Fondazione Telethon is an Italian non-profit biomedical organization committed to advancing research on rare and complex genetic diseases. For over 35 years, it has supported high-impact science aimed at developing innovative treatments and improving the lives of people affected by these conditions. 21% more press release views with Request a Demo

Gene TherapyDrug ApprovalImmunotherapyClinical Study

100 Deals associated with Plerixafor

External Link

KEGG	Wiki	ATC	Drug Bank
D08971	Plerixafor	L03AX16	DB06809

R&D Status

Approved

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
Peripheral Stem Cell Transplantation	France	SEACROSS PHARMACEUTICALS LTD	28 Feb 2023
Hematopoietic stem cell transplantation	Japan	Sanofi KK	19 Dec 2016
Lymphoma	Australia	Sanofi-Aventis Australia Pty Ltd.	18 May 2010
Multiple Myeloma	South Korea	Sanofi-Aventis Korea Co., Ltd.	26 Jan 2010
Stem cell mobilisation	United States	Genzyme Corp.	15 Dec 2008

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Hodgkin's Lymphoma	Phase 3	France	Genzyme Corp.	01 Sep 2008
Hodgkin's Lymphoma	Phase 3	Germany	Genzyme Corp.	01 Sep 2008
Hodgkin's Lymphoma	Phase 3	Italy	Genzyme Corp.	01 Sep 2008
Hodgkin's Lymphoma	Phase 3	Netherlands	Genzyme Corp.	01 Sep 2008
Hodgkin's Lymphoma	Phase 3	Spain	Genzyme Corp.	01 Sep 2008
Hodgkin's Lymphoma	Phase 3	Sweden	Genzyme Corp.	01 Sep 2008
Hodgkin's Lymphoma	Phase 3	United Kingdom	Genzyme Corp.	01 Sep 2008
Refractory Multiple Myeloma	Phase 3	France	Genzyme Corp.	01 Sep 2008
Refractory Multiple Myeloma	Phase 3	Germany	Genzyme Corp.	01 Sep 2008
Refractory Multiple Myeloma	Phase 3	Italy	Genzyme Corp.	01 Sep 2008

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


Tandem Meetings ASTCT and CIBMTR2026	Not Applicable	Multiple Myeloma	138	Plerixafor + double dose G-CSF (Multiple Myeloma)	fjfswinqpd(zjnvkbcajc) = no grade ≥2 adverse reactions occurred with plerixafor, whereas motixafortide was associated with injection-site reactions (grade ≥2, 29.4%; including grade 3, 25%) and grade ≥2 allergic reactions. toqmutesij (ltkwfktmfv ) View more	Positive	04 Feb 2026
Tandem Meetings ASTCT and CIBMTR2026	Not Applicable	Multiple Myeloma	138	Motixafortide +G-CSF (Multiple Myeloma)		Positive	04 Feb 2026
Tandem Meetings ASTCT and CIBMTR2026	Not Applicable	Lymphoma	47	Plerixafor and G-CSF	wtglrdiakp(whbswtcihu) = deqzujvbfb yelngjkxpl (nvxueizevf ) View more	Positive	04 Feb 2026
NCT03746080 (Phase II study of plerixafor combined with whole brain radiation therapy (WBRT) for patients with newly diagnosed glioblastoma, CTgov)	Phase 2	Gliosarcoma \| Glioblastoma Multiforme \| Glioblastoma ... View more	21	Whole-Brain Radiotherapy (WBRT)+Temozolomide+Plerixafor	ufkykgyuqo = hqfdgxbafc rczusdolwb (zjbvyujooy, olbcubghrv - tgdryockiz) View more	-	26 Jun 2024
NCT03746080 (Phase II study of plerixafor combined with whole brain radiation therapy (WBRT) for patients with newly diagnosed glioblastoma, ASCO2024)	Phase 2	Glioblastoma IDH wildtype \| pMGMT unmethylated	17	Plerixafor + WBRT	iwlcjzboyw(prdxsnhkwu) = raameeanaz wxnuystruq (ftbjimzyph ) View more	Negative	24 May 2024
EHA2024	Not Applicable	Multiple Myeloma \| Lymphoma CD34-positive	33	plerixafor (High-volume Apheresis)	xpzpocytgv(xmlgambxhe) = grade I-II diarrhea and myalgias (15%) jzgwsrplea (iqqqlzwhla )	Positive	14 May 2024
NCT04177810 (CTgov)	Phase 2	Metastatic Pancreatic Cancer	25	Cemiplimab+Plerixafor	iutezpmnff = cqzhoesgod pyllmphhei (uwmvtynpog, dlddrfvnms - jhjrzoggzl) View more	-	20 Feb 2024
NCT01696461 (CTgov)	Phase 2	Hodgkin's Lymphoma \| Acute Myeloid Leukemia \| Chronic Lymphocytic Leukemia ... View more	127	Plerixafor	cupttklply = yktnfmfdga lksfxkezoc (ikrwsqzppv, ciwjgdddii - lmdshnnvuz) View more	-	14 Sep 2023
EBMT2023	Not Applicable	-	81	Plerixafor	jjbftcjxqa(czcdzuvdyu) = tzwhfulsey dbfnclzrab (auidawmgfj )	Positive	23 Apr 2023
NCT02231879 (CTgov)	Phase 2/3	Agammaglobulinemia \| Neutropenia \| Myeloproliferative Disorders ... View more	20	G-CSF (G-CSF (Both Periods Combined))	noxcefwjbi(wsfmtrvadf) = lezklajogg vsgabqqnwf (rznogelatp, uuvoxrmlow - etmoqwqkjd)	-	07 Apr 2023
NCT02231879 (CTgov)	Phase 2/3		20	Plerixafor (Plerixafor (Both Periods Combined))	noxcefwjbi(wsfmtrvadf) = ukxvcamncs vsgabqqnwf (rznogelatp, oxcfqzncau - gotihzaqet)	-	07 Apr 2023
EHA2022	Not Applicable	-	84	Plerixafor	qeekbkpccx(sdazcuvnru) = iraugtacsa fpvnfkrnfq (cufghxsizx )	-	12 May 2022

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