Plerixafor

Identification

Summary

Plerixafor is a CXCR4 antagonist used in combination with granulocyte-colony stimulating factor to mobilize hematopoietic stem cells to the peripheral blood for collection and autologous transplantation in patients with non-Hodgkin’s lymphoma and multiple myeloma.

Brand Names

Mozobil

Generic Name

Plerixafor

DrugBank Accession Number

DB06809

Background

Plerixafor is a small-molecule inhibitor of C-X-C chemokine receptor type 4 (CXCR4) that acts as a hematopoietic stem cell mobilizer.^5,9 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.^6,9

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.⁵ 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.³

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.^5,9

Type

Small Molecule

Groups

Approved, Investigational

Structure

Similar Structures

Weight: Average: 502.782
Monoisotopic: 502.447143768
Chemical Formula: C₂₈H₅₄N₈

Synonyms

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

Pharmacology

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.⁹

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Associated Therapies

Mobilization of hematopoietic stem cells

Contraindications & Blackbox Warnings

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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.^7,10 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.⁹

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.⁹

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.^1,2,9

Target	Actions	Organism
AC-X-C chemokine receptor type 4	antagonist inhibitor	Humans

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 (CL_CR). The population pharmacokinetic analysis showed that, with increasing body weight, a mg/kg-based dosage leads to a higher plerixafor exposure (AUC_0-24h). However, NHL patients (<70 kg) given a fixed dose of 20 mg of plerixafor had an AUC_0-10h 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.⁹

Peak concentrations are reached in approximately 30-60 minutes (t_max) following subcutaneous injection.^9,10 In patients given 0.24 mg/kg of plerixafor subcutaneously after receiving 4-days of G-CSF pre-treatment, the C_max and AUC_0-24 were 887 ng/ml and 4337 ng·hr/ml, respectively.¹⁰

Volume of distribution

Plerixafor has an apparent volume of distribution of 0.3 L/kg.⁹

Protein binding

The human plasma protein binding of plerixafor is up to 58%.⁹

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.⁹ 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.¹³

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.⁹

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.⁹ 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.⁴

Clearance

Plerixafor has a total plasma clearance of 4.38 L/h, and a renal clearance of 3.15 L/h.^4,8

Adverse Effects

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Toxicity

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.⁹ 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.⁹ 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/.¹¹

Pathways

Not Available

Pharmacogenomic Effects/ADRs

Not Available

Interactions

Drug Interactions

This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.

Drug	Interaction
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Abacavir	Abacavir may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Aceclofenac	Aceclofenac may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Acemetacin	Acemetacin may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Acetaminophen	Acetaminophen may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Acetazolamide	Acetazolamide may increase the excretion rate of Plerixafor which could result in a lower serum level and potentially a reduction in efficacy.
Acetylsalicylic acid	Acetylsalicylic acid may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Aclidinium	Plerixafor may decrease the excretion rate of Aclidinium which could result in a higher serum level.
Acrivastine	Plerixafor may decrease the excretion rate of Acrivastine which could result in a higher serum level.
Acyclovir	Acyclovir may decrease the excretion rate of Plerixafor which could result in a higher serum level.
Adefovir dipivoxil	Adefovir dipivoxil may decrease the excretion rate of Plerixafor which could result in a higher serum level.

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Food Interactions

No interactions found.

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Product Ingredients

Ingredient	UNII	CAS	InChI Key
Plerixafor octahydrochloride	OD49913540	155148-31-5	UEUPDYPUTTUXLJ-UHFFFAOYSA-N

International/Other Brands

Mozobil (Genzyme Corporation)

Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End
Mozobil	Solution	24 mg/1.2mL	Subcutaneous	Genzyme Corporation	2008-12-15	2018-03-23
Mozobil	Injection, solution	20 mg/ml	Subcutaneous	Genzyme Europe Bv	2020-12-23	Not applicable
Mozobil	Solution	20 mg / mL	Subcutaneous	Sanofi Aventis	2012-03-26	Not applicable
Mozobil	Injection, solution	24 mg/1.2mL	Subcutaneous	sanofi-aventis U.S. LLC	2013-09-01	Not applicable
Plerixafor Accord	Injection, solution	20 mg/ml	Subcutaneous	Accord Healthcare S.L.U.	2023-02-08	Not applicable
Plerixafor Injection	Solution	20 mg / mL	Subcutaneous	Fresenius Kabi	Not applicable	Not applicable
Plerixafor Injection	Solution	20 mg / mL	Subcutaneous	Jamp Pharma Corporation	Not applicable	Not applicable

Chemical Identifiers

UNII: S915P5499N
CAS number: 110078-46-1
InChI Key: YIQPUIGJQJDJOS-UHFFFAOYSA-N
InChI: InChI=1S/C28H54N8/c1-9-29-15-17-31-13-3-21-35(23-19-33-11-1)25-27-5-7-28(8-6-27)26-36-22-4-14-32-18-16-30-10-2-12-34-20-24-36/h5-8,29-34H,1-4,9-26H2
IUPAC Name: 1-({4-[(1,4,8,11-tetraazacyclotetradecan-1-yl)methyl]phenyl}methyl)-1,4,8,11-tetraazacyclotetradecane
SMILES: C(N1CCCNCCNCCCNCC1)C1=CC=C(CN2CCCNCCNCCCNCC2)C=C1

References

Synthesis Reference

Xu, D., et al. (1997). Process for preparing 1,1'-[1,4-phenylenebis-(methylene)]-bis-1,4,8,11-tetraazacyclotetradecane (U.S. Patent No. 5,612,478 A). U.S. Patent and Trademark Office. https://patentimages.storage.googleapis.com/23/2a/c4/cdec2e80dbe460/US5612478.pdf

General References

Uy GL, Rettig MP, Cashen AF: Plerixafor, a CXCR4 antagonist for the mobilization of hematopoietic stem cells. Expert Opin Biol Ther. 2008 Nov;8(11):1797-804. doi: 10.1517/14712598.8.11.1797 . [Article]
Fricker SP: A novel CXCR4 antagonist for hematopoietic stem cell mobilization. Expert Opin Investig Drugs. 2008 Nov;17(11):1749-60. doi: 10.1517/13543784.17.11.1749 . [Article]
DiPersio JF, Stadtmauer EA, Nademanee A, Micallef IN, Stiff PJ, Kaufman JL, Maziarz RT, 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 4;113(23):5720-6. doi: 10.1182/blood-2008-08-174946. Epub 2009 Apr 10. [Article]
Stewart DA, Smith C, MacFarland R, Calandra G: Pharmacokinetics and pharmacodynamics of plerixafor in patients with non-Hodgkin lymphoma and multiple myeloma. Biol Blood Marrow Transplant. 2009 Jan;15(1):39-46. doi: 10.1016/j.bbmt.2008.10.018. [Article]
Brave M, Farrell A, Ching Lin S, Ocheltree T, Pope Miksinski S, Lee SL, 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. 2010;78(3-4):282-8. doi: 10.1159/000315736. Epub 2010 Jun 8. [Article]
Choi HY, Yong CS, Yoo BK: Plerixafor for stem cell mobilization in patients with non-Hodgkin's lymphoma and multiple myeloma. Ann Pharmacother. 2010 Jan;44(1):117-26. doi: 10.1345/aph.1M380. Epub 2009 Dec 15. [Article]
Keating GM: Plerixafor: a review of its use in stem-cell mobilization in patients with lymphoma or multiple myeloma. Drugs. 2011 Aug 20;71(12):1623-47. doi: 10.2165/11206040-000000000-00000. [Article]
MacFarland R, Hard ML, Scarborough R, Badel K, Calandra G: A pharmacokinetic study of plerixafor in subjects with varying degrees of renal impairment. Biol Blood Marrow Transplant. 2010 Jan;16(1):95-101. doi: 10.1016/j.bbmt.2009.09.003. Epub 2009 Sep 10. [Article]
FDA Approved Drug Products: MOZOBIL (plerixafor) injection for subcutaneous use (August 2020) [Link]
EMA Summary of Product Characteristics: Mozobil (plerixafor) injection solution for subcutaneous use (April 2014) [Link]
FDA Pharmacology Review: Mozobil (plerixafor) injection (December 2008) [Link]
Toronto Research Chemicals: Plerixafor SDS [Link]
CHMP Assessment Report: Mozobil (plerixafor) [Link]

External Links

Human Metabolome Database: HMDB0015681
KEGG Drug: D08971
PubChem Compound: 65015
PubChem Substance: 99443297
ChemSpider: 58531
BindingDB: 50035696
RxNav: 733003
ChEBI: 125354
ChEMBL: CHEMBL18442
ZINC: ZINC000022443609
PharmGKB: PA165958410
Guide to Pharmacology: GtP Drug Page
RxList: RxList Drug Page
Drugs.com: Drugs.com Drug Page
Wikipedia: Plerixafor

Clinical Trials

Clinical Trials

Phase	Status	Purpose	Conditions	Count
4	Completed	Treatment	Autologous Haematopoietic Stem Cell Transplant	1
4	Completed	Treatment	Diabetes	1
4	Completed	Treatment	Non-Hodgkin's Lymphoma (NHL) / Non-Hodgkin's Lymphomas	1
4	Recruiting	Treatment	Lymphoma	1
4	Unknown Status	Treatment	Autologous Stem Cell Transplantation	1
3	Completed	Treatment	Front Line Mobilization / Hodgkin's Disease or Multiple Myeloma / Non-Hodgkin's Lymphoma (NHL) / Transplantations	1
3	Completed	Treatment	Multiple Myeloma (MM)	2
3	Completed	Treatment	Non-Hodgkin's Lymphoma (NHL)	1
3	Completed	Treatment	Non-Hodgkin's Lymphoma (NHL) / Non-Hodgkin's Lymphomas	1
3	Terminated	Treatment	Refractory Multiple Myeloma	1

Pharmacoeconomics

Manufacturers

Not Available

Packagers

Not Available

Dosage Forms

Form	Route	Strength
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
Injection, solution		20 mg/ml
Solution	Subcutaneous
Solution	Subcutaneous	20 mg/ml
Injection, solution	Subcutaneous	20 mg/ml
Solution	Subcutaneous	24 mg
Injection, solution		20 mg/1ml
Solution	Subcutaneous	20 mg/1ml

Prices

Not Available

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)
US6987102	No	2006-01-17	2023-07-22
US7897590	No	2011-03-01	2023-03-22
USRE42152	No	2011-02-15	2018-12-10

Properties

State

Solid

Experimental Properties

Property	Value	Source
melting point (°C)	131.5 °C	FDA label
water solubility	Slightly soluble	SDS
pKa	8.5-11.5 and <2.4	CHMP Assessment Report

Predicted Properties

Property	Value	Source
Water Solubility	0.0472 mg/mL	ALOGPS
logP	0.62	ALOGPS
logP	-0.43	Chemaxon
logS	-4	ALOGPS
pKa (Strongest Basic)	10.23	Chemaxon
Physiological Charge	4	Chemaxon
Hydrogen Acceptor Count	8	Chemaxon
Hydrogen Donor Count	6	Chemaxon
Polar Surface Area	78.66 Å²	Chemaxon
Rotatable Bond Count	4	Chemaxon
Refractivity	155.01 m³·mol^-1	Chemaxon
Polarizability	60.65 Å³	Chemaxon
Number of Rings	3	Chemaxon
Bioavailability	0	Chemaxon
Rule of Five	No	Chemaxon
Ghose Filter	No	Chemaxon
Veber's Rule	No	Chemaxon
MDDR-like Rule	No	Chemaxon

Predicted ADMET Features

Property	Value	Probability
Human Intestinal Absorption	+	0.932
Blood Brain Barrier	+	0.6867
Caco-2 permeable	-	0.5403
P-glycoprotein substrate	Substrate	0.8076
P-glycoprotein inhibitor I	Non-inhibitor	0.8119
P-glycoprotein inhibitor II	Non-inhibitor	0.7683
Renal organic cation transporter	Inhibitor	0.5069
CYP450 2C9 substrate	Non-substrate	0.8905
CYP450 2D6 substrate	Substrate	0.5274
CYP450 3A4 substrate	Non-substrate	0.7818
CYP450 1A2 substrate	Non-inhibitor	0.8787
CYP450 2C9 inhibitor	Non-inhibitor	0.9272
CYP450 2D6 inhibitor	Non-inhibitor	0.7149
CYP450 2C19 inhibitor	Non-inhibitor	0.9114
CYP450 3A4 inhibitor	Non-inhibitor	0.8817
CYP450 inhibitory promiscuity	Low CYP Inhibitory Promiscuity	0.926
Ames test	Non AMES toxic	0.7906
Carcinogenicity	Non-carcinogens	0.9106
Biodegradation	Not ready biodegradable	0.9824
Rat acute toxicity	2.1178 LD50, mol/kg	Not applicable
hERG inhibition (predictor I)	Weak inhibitor	0.5
hERG inhibition (predictor II)	Inhibitor	0.6334

ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397)

Spectra

Mass Spec (NIST)

Not Available

Spectra

Spectrum	Spectrum Type	Splash Key
Predicted GC-MS Spectrum - GC-MS	Predicted GC-MS	Not Available
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	Not Available

Targets

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Property	Measurement	pH	Temperature (°C)	References
IC 50 (nM)	0.81	N/A	N/A	A30678
IC 50 (nM)	15200	N/A	N/A	A30680
IC 50 (nM)	245	N/A	N/A	A30679
IC 50 (nM)	27.4	N/A	N/A	A30680
IC 50 (nM)	289.1	N/A	N/A	A30681
IC 50 (nM)	74	N/A	N/A	A29332
Ki (nM)	220	N/A	N/A	A30677
Ki (nM)	890	N/A	N/A	A30677

Details1. C-X-C chemokine receptor type 4

Kind: Protein
Organism: Humans
Pharmacological action: Yes
Actions: Antagonist
Inhibitor

General Function: Virus receptor activity
Specific Function: 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. Acts as a receptor for extracellular ubiq...
Gene Name: CXCR4
Uniprot ID: P61073
Uniprot Name: C-X-C chemokine receptor type 4
Molecular Weight: 39745.055 Da

References

Uy GL, Rettig MP, Cashen AF: Plerixafor, a CXCR4 antagonist for the mobilization of hematopoietic stem cells. Expert Opin Biol Ther. 2008 Nov;8(11):1797-804. doi: 10.1517/14712598.8.11.1797 . [Article]
Jujo K, Ii M, Sekiguchi H, Klyachko E, Misener S, Tanaka T, Tongers J, Roncalli J, Renault MA, Thorne T, Ito A, Clarke T, Kamide C, Tsurumi Y, Hagiwara N, Qin G, Asahi M, Losordo DW: CXC-chemokine receptor 4 antagonist AMD3100 promotes cardiac functional recovery after ischemia/reperfusion injury via endothelial nitric oxide synthase-dependent mechanism. Circulation. 2013 Jan 1;127(1):63-73. doi: 10.1161/CIRCULATIONAHA.112.099242. Epub 2012 Nov 30. [Article]
Pan C, Liu P, Ma D, Zhang S, Ni M, Fang Q, Wang J: Bone marrow mesenchymal stem cells in microenvironment transform into cancer-associated fibroblasts to promote the progression of B-cell acute lymphoblastic leukemia. Biomed Pharmacother. 2020 Oct;130:110610. doi: 10.1016/j.biopha.2020.110610. Epub 2020 Aug 12. [Article]
FDA Approved Drug Products: MOZOBIL (plerixafor) injection for subcutaneous use (August 2020) [Link]

Drug created at September 14, 2010 16:21 / Updated at March 30, 2023 19:23

Plerixafor

Identification

Structure for Plerixafor (DB06809)

Pharmacology

Interactions

Products

Categories

Chemical Identifiers

References

Clinical Trials

Pharmacoeconomics

Properties

Spectra

Targets

References