Plerixafor 24mg/1.2ml solution for injection vials
Prescription only
Requires a prescription from a doctor or prescriber
Anaemias and some other blood disorders
Active ingredients:
Plerixafor
No active safety alerts
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
Source: MHRA Products DatabaseOGL 3.0
Updated 3 months ago(16 Jan 2026)Safety monitoring data
Yellow Card reports
MHRA
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
EMA
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Suspected adverse reactions reported for Plerixafor
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
6 branded products available
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Plerixafor 24mg/1.2ml solution for injection vials
Plerixafor 24mg/1.2ml solution for injection vials
Plerixafor 24mg/1.2ml solution for injection vials
Plerixafor 24mg/1.2ml solution for injection vials
Plerixafor 24mg/1.2ml solution for injection vials
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WHO defined daily dose (DDD)
16.8 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
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Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Clinical guidelines and formulary information
British National Formulary
Plerixafor
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
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Supply & product information
Official product databases and supply status monitoring
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Codes for healthcare professionals and prescribing systems
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These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
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Searching UK clinical trials...
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
0.3 hours
Mechanism
Plerixafor inhibits the C-X-C chemokine receptor type 4 (CXCR4) on CD34+ cells a…
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
0.04 mg/k
Plerixafor follows a two-compartment pharmacokinetic profile with first-order absorption and exhibits linear kinetics between 0.04…
Half-life
0.3 hours
Plerixafor has a distribution half-life of 0.3 hours and a terminal population half-life of 5.3…
Protein binding
58%
The human plasma protein binding of plerixafor is up to 58%.
[L45678]
[L45678]
Volume of distribution
0.3 L/kg
Plerixafor has an apparent volume of distribution of 0.3 L/kg.
[L45678]
[L45678]
Metabolism
Plerixafor is not metabolized by the liver and is not a metabolism-dependent inhibitor of major cytochrome P450 enzymes, including 1A2, 2C9, 2C19, 2D6 and 3A4.…
Elimination
0.24 mg/k
Plerixafor is mainly eliminated through urine. In healthy volunteers with normal renal function given 0.24…
Clearance
4.38 L/h
Plerixafor has a total plasma clearance of 4.38 L/h, and a renal clearance of 3.15 L/h.
[A7116][A258423]
[A7116][A258423]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Plerixafor is a small-molecule inhibitor of C-X-C chemokine receptor type 4 (CXCR4) that acts as a hematopoietic stem cell mobilizer.[A7117][L45678] It is used to stimulate the release of stem cells from the bone marrow into the blood in patients with non-Hodgkin's lymphoma (NHL) and multiple myeloma to stimulate their immune system. These stem cells are then collected and used in autologous stem cell transplantation to replace blood-forming cells destroyed by chemotherapy.[A7118][L45678]
As an inhibitor of CXCR4, plerixafor blocks the binding of its ligand, stromal cell-derived factor-1-alpha (SDF-1α). Since CXCR4 and SDF-1α are involved in the trafficking and homing of CD34+ cells to the marrow compartment, blocking this interaction leads to an increase in CD34+ cell circulating levels.[A7117] Compared to placebo with G-CSF, the plerixafor and G-CSF mobilization regimen has a higher probability of achieving the optimal CD34+ cell target for tandem transplantation in fewer apheresis procedures.[A7115]
Plerixafor has orphan drug status in the United States and European Union and was approved by the US Food and Drug Administration on December 15, 2008.[A7117][L45678]
As an inhibitor of CXCR4, plerixafor blocks the binding of its ligand, stromal cell-derived factor-1-alpha (SDF-1α). Since CXCR4 and SDF-1α are involved in the trafficking and homing of CD34+ cells to the marrow compartment, blocking this interaction leads to an increase in CD34+ cell circulating levels.[A7117] Compared to placebo with G-CSF, the plerixafor and G-CSF mobilization regimen has a higher probability of achieving the optimal CD34+ cell target for tandem transplantation in fewer apheresis procedures.[A7115]
Plerixafor has orphan drug status in the United States and European Union and was approved by the US Food and Drug Administration on December 15, 2008.[A7117][L45678]
Properties:
solid
Avg. mass: 502.78 Da
DrugBank indication
Plerixafor is indicated in combination with granulocyte-colony stimulating factor (G-CSF) to mobilize hematopoietic stem cells (HSCs) to the peripheral blood for collection and subsequent autologous transplantation in patients with non-Hodgkin’s lymphoma or multiple myeloma.
[L45678]
[L45678]
Also known as(17)
1,1'-(1,4-phenylenebis(methylene))bis-1,4,8,11-tetraazacyclotetradecane
1,4,8,11-tetraazacyclotetradecane, 1,1'-(1,4-phenylenebis(methylene))bis-
Plerixafor
CXC-R4
CXCR-4
FB22
Fusin
HM89
Dosage forms(14)
Solution (Subcutaneous) — 24.000 mg
(Subcutaneous) — 20 mg/ml
Injection, solution (Parenteral; Subcutaneous) — 20 MG/ML
Injection, solution (Subcutaneous) — 24 mg/1.2mL
Solution (Subcutaneous) — 20 mg / mL
Solution (Subcutaneous) — 24 mg/1.2mL
Solution (Subcutaneous) — 20 mg/ml
Injection, solution (Subcutaneous) — 20 mg/ml
Molecular properties(18)
Drug interactions(732)
Known interactions with other medications. Always consult a healthcare professional.
Cyclosporine
Moderate
Cyclosporine may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Icosapent may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Cefotiam may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Mesalazine
Moderate
Mesalazine may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Cefmenoxime
Moderate
Cefmenoxime may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Cefmetazole
Moderate
Cefmetazole may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Pamidronic acid
Moderate
Pamidronic acid may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Tenofovir disoproxil
Moderate
Tenofovir disoproxil may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Indomethacin
Moderate
Indomethacin may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Cidofovir may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Cefpiramide
Moderate
Cefpiramide may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Ceftazidime
Moderate
Ceftazidime may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Loracarbef
Moderate
Loracarbef may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Cefalotin may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Nabumetone
Moderate
Nabumetone may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Ketorolac may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Tenoxicam may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Celecoxib may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Cefotaxime
Moderate
Cefotaxime may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Tolmetin may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Foscarnet may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Rofecoxib may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Piroxicam may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Methotrexate
Moderate
Methotrexate may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Cephalexin
Moderate
Cephalexin may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Fenoprofen
Moderate
Fenoprofen may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Valaciclovir
Moderate
Valaciclovir may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Valdecoxib
Moderate
Valdecoxib may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Diclofenac
Moderate
Diclofenac may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Sulindac may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Bacitracin
Moderate
Bacitracin may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Amphotericin B
Moderate
Amphotericin B may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Cephaloglycin
Moderate
Cephaloglycin may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Flurbiprofen
Moderate
Flurbiprofen may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Adefovir dipivoxil
Moderate
Adefovir dipivoxil may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Pentamidine
Moderate
Pentamidine may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Etodolac may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Mefenamic acid
Moderate
Mefenamic acid may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Acyclovir may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Naproxen may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Sulfasalazine
Moderate
Sulfasalazine may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Phenylbutazone
Moderate
Phenylbutazone may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Meloxicam may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Carprofen may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Cefaclor may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Diflunisal
Moderate
Diflunisal may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Tacrolimus
Moderate
Tacrolimus may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Ceforanide
Moderate
Ceforanide may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Salicylic acid
Moderate
Salicylic acid may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Meclofenamic acid
Moderate
Meclofenamic acid may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Showing 50 of 732 interactions
Toxicity & overdose
There is limited data about the effects of plerixafor at doses higher than the recommended (0.24 mg/kg subcutaneously). However, the frequency of gastrointestinal disorders, vasovagal reactions, orthostatic hypotension, and/or syncope may be higher.
[L45678]
The carcinogenicity of plerixafor has not been evaluated, and the effect of plerixafor on human fertility is unknown. According to the results from an in vitro bacterial mutation assay, an in vitro chromosomal aberration test, and an in vivo bone marrow micronucleus test in rats after subcutaneous doses up to 25 mg/kg, plerixafor is not genotoxic.
[L45678]
In mice and rats, the LD50 of plerixafor by intravenous injection is 5 mg/kg.
The LD50 of plerixafor by subcutaneous injection is 16 mg/kg in mice and >50 mg/kg in rats/.
[L45688]
[L45678]
The carcinogenicity of plerixafor has not been evaluated, and the effect of plerixafor on human fertility is unknown. According to the results from an in vitro bacterial mutation assay, an in vitro chromosomal aberration test, and an in vivo bone marrow micronucleus test in rats after subcutaneous doses up to 25 mg/kg, plerixafor is not genotoxic.
[L45678]
In mice and rats, the LD50 of plerixafor by intravenous injection is 5 mg/kg.
The LD50 of plerixafor by subcutaneous injection is 16 mg/kg in mice and >50 mg/kg in rats/.
[L45688]
How it works
Mechanism of action
Plerixafor inhibits the C-X-C chemokine receptor type 4 (CXCR4) on CD34+ cells and reversibly blocks the binding of its ligand, stromal cell-derived factor-1-alpha (SDF-1α). SDF-1α and CXCR4 play a role in the trafficking and homing of human hematopoietic stem cells (HSCs) to the marrow compartment. In the marrow, stem cell CXCR4 can help anchor HSCs to the marrow matrix, either directly via SDF-1α or through the induction of other adhesion molecules. By blocking the interaction between SDF-1α and CXCR4 with plerixafor, the mobilization of progenitor cells is triggered. Adding granulocyte-colony stimulating factor (G-CSF) to enhance CD34+ cell mobilization increases the yield of stem cells, an important determinant of graft adequacy.[A7113][A7114][L45678]
Pharmacodynamics
Plerixafor is a bicyclam derivative that antagonizes C-X-C chemokine receptor type 4 (CXCR4) by binding to three acidic residues in the ligand-binding pocket: Asp171, Asp262, and Glu288.[A7119][L45683] Blood levels of CD34+ cells peaked between 6 and 9 hours after the administration of 0.24 mg/kg plerixafor in healthy subjects. In combination with a granulocyte-colony stimulating factor (G-CSF), circulating CD34+ cells in the peripheral blood peaked between 10 and 14 hours. The use of plerixafor is not associated with QT/QTc prolongation at single doses up to 0.40 mg/kg.[L45678]
Serious hypersensitivity reactions, such as anaphylactic-type reactions, have occurred in patients receiving plerixafor. The use of plerixafor may also cause tumor cell mobilization in leukemia patients, splenic enlargement and rupture, embryo-fetal toxicity, and hematologic effects, such as leukocytosis and thrombocytopenia. When used in combination with G-CSF for hematopoietic stem cell mobilization‚ plerixafor may lead to the release of tumor cells from the marrow and their subsequent collection in the leukapheresis product.[L45678]
Serious hypersensitivity reactions, such as anaphylactic-type reactions, have occurred in patients receiving plerixafor. The use of plerixafor may also cause tumor cell mobilization in leukemia patients, splenic enlargement and rupture, embryo-fetal toxicity, and hematologic effects, such as leukocytosis and thrombocytopenia. When used in combination with G-CSF for hematopoietic stem cell mobilization‚ plerixafor may lead to the release of tumor cells from the marrow and their subsequent collection in the leukapheresis product.[L45678]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Plerixafor follows a two-compartment pharmacokinetic profile with first-order absorption and exhibits linear kinetics between 0.04 mg/kg and 0.24 mg/kg. The pharmacokinetic profile of plerixafor in healthy subjects was similar to the one observed in patients with non-Hodgkin’s lymphoma (NHL) and multiple myeloma (MM) who received plerixafor in combination with granulocyte-colony stimulating factor (G-CSF). In addition, the clearance of plerixafor has a significant relationship with creatinine clearance (CLCR).
The population pharmacokinetic analysis showed that, with increasing body weight, a mg/kg-based dosage leads to a higher plerixafor exposure (AUC0-24h). However, NHL patients (<70 kg) given a fixed dose of 20 mg of plerixafor had an AUC0-10h 1.43-fold higher than the one detected in patients given 0.24 mg/kg of plerixafor. Therefore, a body weight of 83 kg was selected as an appropriate cut-off point to transition patients from fixed to weight-based dosing.
[L45678]
Peak concentrations are reached in approximately 30-60 minutes (tmax) following subcutaneous injection.
[L45678][L45683]
In patients given 0.24 mg/kg of plerixafor subcutaneously after receiving 4-days of G-CSF pre-treatment, the Cmax and AUC0-24 were 887 ng/ml and 4337 ng·hr/ml, respectively.
[L45683]
The population pharmacokinetic analysis showed that, with increasing body weight, a mg/kg-based dosage leads to a higher plerixafor exposure (AUC0-24h). However, NHL patients (<70 kg) given a fixed dose of 20 mg of plerixafor had an AUC0-10h 1.43-fold higher than the one detected in patients given 0.24 mg/kg of plerixafor. Therefore, a body weight of 83 kg was selected as an appropriate cut-off point to transition patients from fixed to weight-based dosing.
[L45678]
Peak concentrations are reached in approximately 30-60 minutes (tmax) following subcutaneous injection.
[L45678][L45683]
In patients given 0.24 mg/kg of plerixafor subcutaneously after receiving 4-days of G-CSF pre-treatment, the Cmax and AUC0-24 were 887 ng/ml and 4337 ng·hr/ml, respectively.
[L45683]
Half-life
Plerixafor has a distribution half-life of 0.3 hours and a terminal population half-life of 5.3 hours in patients with normal renal function. In studies with healthy subjects and patients, the terminal half-life in plasma ranges between 3 and 5 hours.
[L45678]
In patients with non-Hodgkin lymphoma, the terminal half-life of plerixafor is 4.4 hours, and in patients with multiple myeloma, the terminal half-life is 5.6 hours.
[A7116]
[L45678]
In patients with non-Hodgkin lymphoma, the terminal half-life of plerixafor is 4.4 hours, and in patients with multiple myeloma, the terminal half-life is 5.6 hours.
[A7116]
Protein binding
The human plasma protein binding of plerixafor is up to 58%.
[L45678]
[L45678]
Volume of distribution
Plerixafor has an apparent volume of distribution of 0.3 L/kg.
[L45678]
[L45678]
Metabolism
Plerixafor is not metabolized by the liver and is not a metabolism-dependent inhibitor of major cytochrome P450 enzymes, including 1A2, 2C9, 2C19, 2D6 and 3A4. In addition, it does not induce cytochrome P450 1A2, 2B6, or 3A4 enzymes.
[L45678]
Plerixafor is metabolically stable, and in vivo studies in rats and dogs showed that the non-parent radiolabelled components in plasma and urine were Cu2+ complexes with plerixafor. This is consistent with the presence of two cyclam rings in plerixafor, which may act as potential chelating sites.
[L45713]
[L45678]
Plerixafor is metabolically stable, and in vivo studies in rats and dogs showed that the non-parent radiolabelled components in plasma and urine were Cu2+ complexes with plerixafor. This is consistent with the presence of two cyclam rings in plerixafor, which may act as potential chelating sites.
[L45713]
Route of elimination
Plerixafor is mainly eliminated through urine. In healthy volunteers with normal renal function given 0.24 mg/kg of plerixafor, approximately 70% of the parent drug is excreted in urine in the first 24 hours. An in vitro study with MDCKII and MDCKII-MDR1 cell models found that plerixafor is not a substrate or inhibitor of P-glycoprotein.
[L45678]
[L45678]
Clearance
Plerixafor has a total plasma clearance of 4.38 L/h, and a renal clearance of 3.15 L/h.
[A7116][A258423]
[A7116][A258423]
Drug targets(1)
Proteins and enzymes this drug interacts with in the body
C-X-C chemokine receptor type 4
CXCR4
antagonist
inhibitor
Specific functionactin binding
Cellular location
Cell membrane
General function & pharmacology
Receptor for the C-X-C chemokine CXCL12/SDF-1 that transduces a signal by increasing intracellular calcium ion levels and enhancing MAPK1/MAPK3 activation .
PMID:10452968 PMID:18799424 PMID:24912431 PMID:28978524
Involved in the AKT signaling cascade .
PMID:24912431
Plays a role in regulation of cell migration, e.g. during wound healing .
PMID:28978524
Acts as a receptor for extracellular ubiquitin; leading to enhanced intracellular calcium ions and reduced cellular cAMP levels .
PMID:20228059
Binds bacterial lipopolysaccharide (LPS) et mediates LPS-induced inflammatory response, including TNF secretion by monocytes .
PMID:11276205
Involved in hematopoiesis and in cardiac ventricular septum formation. Also plays an essential role in vascularization of the gastrointestinal tract, probably by regulating vascular branching and/or remodeling processes in endothelial cells. Involved in cerebellar development.
In the CNS, could mediate hippocampal-neuron survival (By similarity)
PMID:10452968 PMID:18799424 PMID:24912431 PMID:28978524
Involved in the AKT signaling cascade .
PMID:24912431
Plays a role in regulation of cell migration, e.g. during wound healing .
PMID:28978524
Acts as a receptor for extracellular ubiquitin; leading to enhanced intracellular calcium ions and reduced cellular cAMP levels .
PMID:20228059
Binds bacterial lipopolysaccharide (LPS) et mediates LPS-induced inflammatory response, including TNF secretion by monocytes .
PMID:11276205
Involved in hematopoiesis and in cardiac ventricular septum formation. Also plays an essential role in vascularization of the gastrointestinal tract, probably by regulating vascular branching and/or remodeling processes in endothelial cells. Involved in cerebellar development.
In the CNS, could mediate hippocampal-neuron survival (By similarity)
Scientific references(8)
Uy G.L., Rettig M.P., Cashen A.F.
Plerixafor, a CXCR4 antagonist for the mobilization of hematopoietic stem cells.
Expert Opinion Biological Therapeutics
2008 Nov8(11):1797-804. doi: 10.1517/14712598.8.11.1797
Fricker S.P.
A novel CXCR4 antagonist for hematopoietic stem cell mobilization.
Expert Opinion Investig Drugs
2008 Nov17(11):1749-60. doi: 10.1517/13543784.17.11.1749
DiPersio J.F., Stadtmauer E.A., Nademanee A., Micallef I.N., Stiff P.J., Kaufman J.L., Maziarz R.T., Hosing C., Fruehauf S., Horwitz M., Cooper D., Bridger G., Calandra G.
Plerixafor and G-CSF versus placebo and G-CSF to mobilize hematopoietic stem cells for autologous stem cell transplantation in patients with multiple myeloma.
Blood
2009 Jun 4113(23):5720-6. doi: 10.1182/blood-2008-08-174946. Epub 2009 Apr 10
Stewart D.A., Smith C., MacFarland R., Calandra G.
Pharmacokinetics and pharmacodynamics of plerixafor in patients with non-Hodgkin lymphoma and multiple myeloma.
Biological Blood Marrow Transplant
2009 Jan15(1):39-46. doi: 10.1016/j.bbmt.2008.10.018
Brave M., Farrell A., Ching Lin S., Ocheltree T., Pope Miksinski S., Lee S.L., Saber H., Fourie J., Tornoe C., Booth B., Yuan W., He K., Justice R., Pazdur R.
FDA review summary: Mozobil in combination with granulocyte colony-stimulating factor to mobilize hematopoietic stem cells to the peripheral blood for collection and subsequent autologous transplantation.
Oncology
201078(3-4):282-8. doi: 10.1159/000315736. Epub 2010 Jun 8
Choi H.Y., Yong C.S., Yoo B.K.
Plerixafor for stem cell mobilization in patients with non-Hodgkin's lymphoma and multiple myeloma.
Ann Pharmacother
2010 Jan44(1):117-26. doi: 10.1345/aph.1M380. Epub 2009 Dec 15
Keating G.M.
Plerixafor: a review of its use in stem-cell mobilization in patients with lymphoma or multiple myeloma.
Drugs
2011 Aug 2071(12):1623-47. doi: 10.2165/11206040-000000000-00000
MacFarland R., Hard M.L., Scarborough R., Badel K., Calandra G.
A pharmacokinetic study of plerixafor in subjects with varying degrees of renal impairment.
Biological Blood Marrow Transplant
2010 Jan16(1):95-101. doi: 10.1016/j.bbmt.2009.09.003. Epub 2009 Sep 10
ATC classification(1 code)
ATC L03AX16
Affected organisms(1)
Humans and other mammals
International brands(1)
Salt forms(1)
Plerixafor octahydrochloride(DBSALT002325)
Experimental properties(3)
Protein Data Bank entries(1)
Commercial products(20)
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Plerixafor
Additional database identifiers
Drugs Product Database (DPD)
21077
ChemSpider
58531
BindingDB
50035696
PDB
VH6
Guide to Pharmacology
844
ZINC
ZINC000022443609
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2561
GenAtlas
CXCR4
GeneCards
CXCR4
GenBank Gene Database
L01639
GenBank Protein Database
189314
Guide to Pharmacology
71
UniProt Accession
CXCR4_HUMAN
Patent information
All patents expired, 3 expired
6987102
United States
Approved 17 Jan 2006 · Expires 22 Jul 2023
Expired
7897590
United States
Approved 1 Mar 2011 · Expires 22 Mar 2023
Expired
RE42152
United States
Approved 15 Feb 2011 · Expires 10 Dec 2018
Expired
Patent protection has expired — generic versions may be available.
Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated about 1 month ago(4 Mar 2026)