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These highlights do not include all the information needed to use MOZOBIL safely and effectively. See full prescribing information for MOZOBIL. MOZOBIL (plerixafor injection), Solution for Subcutaneous use Initial U.S. Approval: | Mozobil

05:42 EDT 27th August 2014 | BioPortfolio

Note: While we endeavour to keep our records up-to-date one should not rely on these details being accurate without first consulting a professional. Click here to read our full medical disclaimer.

Mozobil (plerixafor injection) is indicated in combination with granulocyte-colony stimulating factor (G-CSF) to mobilize hematopoietic stem cells to the peripheral blood for collection and subsequent autologous transplantation in patients with non-Hodgkin’s lymphoma (NHL) and multiple myeloma (MM).

Vials should be inspected visually for particulate matter and discoloration prior to administration and should not be used if there is particulate matter or if the solution is discolored.

Begin treatment with Mozobil after the patient has received G-CSF once daily for four days.  [see Dosage and Administration (2.2) ]  Administer Mozobil approximately 11 hours prior to initiation of each apheresis for up to 4 consecutive days.

The recommended dose of Mozobil is 0.24 mg/kg body weight by subcutaneous (SC) injection. Use the patient’s actual body weight to calculate the volume of Mozobil to be administered. Each vial delivers 1.2 mL of 20 mg/mL solution, and the volume to be administered to patients should be calculated from the following equation:

    0.012 X patient’s actual body weight (in kg) = volume to be administered (in mL)

In clinical studies, Mozobil dose has been calculated based on actual body weight in patients up to 175% of ideal body weight. Mozobil dose and treatment of patients weighing more than 175% of ideal body weight have not been investigated.

Based on increasing exposure with increasing body weight, the plerixafor dose should not exceed 40 mg/day.  [see Clinical Pharmacology (12.3) ]  

Administer daily morning doses of G-CSF 10 micrograms/kg for 4 days prior to the first evening dose of Mozobil and on each day prior to apheresis. [see Clinical Studies (14) ]

In patients with moderate and severe renal impairment (estimated creatinine clearance (CL) ≤ 50 mL/min), reduce the dose of Mozobil by one-third to 0.16 mg/kg as shown in Table 1. If CL is ≤ 50 mL/min the dose should not exceed 27 mg/day, as the mg/kg-based dosage results in increased plerixafor exposure with increasing body weight.  [see Clinical Pharmacology (12.3) ]   Similar systemic exposure is predicted if the dose is reduced by one-third in patients with moderate and severe renal impairment compared with subjects with normal renal function.  [see Clinical Pharmacology (12.3) ]  

The following (Cockroft-Gault) formula may be used to estimate CL: 

    Males:    Creatinine clearance (mL/min) = weight (kg) X (140 – age in years)                                                             72 X serum creatinine (mg/dL)

    Females:    Creatinine clearance (mL/min) = 0.85 X value calculated for males

There is insufficient information to make dosage recommendations in patients on hemodialysis.

Table 1: Recommended Dosage of Plerixafor in Patients with Renal Impairment
     Estimated Creatinine Clearance    
(mL/min)
Dose
> 50     0.24 mg/kg once daily (not to exceed 40 mg/day)     
≤ 50     0.16 mg/kg once daily (not to exceed 27 mg/day)     

Single-use vial containing 1.2 mL of a 20 mg/mL solution.

None

For the purpose of HSC mobilization, Mozobil may cause mobilization of leukemic cells and subsequent contamination of the apheresis product. Therefore, Mozobil is not intended for HSC mobilization and harvest in patients with leukemia.

Leukocytosis Administration of Mozobil in conjunction with G-CSF increases circulating leukocytes as well as HSC populations. Monitor white blood cell counts during Mozobil use. Exercise clinical judgment when administering Mozobil to patients with peripheral blood neutrophil counts above 50,000/mcL.

Thrombocytopenia Thrombocytopenia has been observed in patients receiving Mozobil. Monitor platelet counts in all patients who receive Mozobil and then undergo apheresis.

When Mozobil is used in combination with G-CSF for HSC mobilization‚ tumor cells may be released from the marrow and subsequently collected in the leukapheresis product. The effect of potential reinfusion of tumor cells has not been well-studied.

Higher absolute and relative spleen weights associated with extramedullary hematopoiesis were observed following prolonged (2 to 4 weeks) daily plerixafor SC administration in rats at doses approximately 4-fold higher than the recommended human dose based on body surface area. The effect of Mozobil on spleen size in patients was not specifically evaluated in clinical studies. Evaluate individuals receiving Mozobil in combination with G-CSF who report left upper abdominal pain and/or scapular or shoulder pain for splenic integrity.

Pregnancy Category D Mozobil may cause fetal harm when administered to a pregnant woman. Plerixafor was teratogenic in animals. There are no adequate and well-controlled studies in pregnant women using Mozobil. Women of childbearing potential should be advised to avoid becoming pregnant while receiving treatment with Mozobil. If this drug is used during pregnancy, or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to the fetus.  [see Use In Specific Populations (8.1) ]

The following serious adverse reactions are discussed elsewhere in the labeling:

The most common adverse reactions (≥ 10%) reported in patients who received Mozobil in conjunction with G-CSF regardless of causality and more frequent with Mozobil than placebo during HSC mobilization and apheresis were diarrhea, nausea, fatigue, injection site reactions, headache, arthralgia, dizziness, and vomiting.

Safety data for Mozobil in combination with G-CSF were obtained from two randomized placebo-controlled studies (301 patients) and 10 uncontrolled studies (242 patients). Patients were primarily treated with Mozobil at daily doses of 0.24 mg/kg SC. Median exposure to Mozobil in these studies was 2 days (range 1 to 7 days).

In the two randomized studies in patients with NHL and MM, a total of 301 patients were treated in the Mozobil and G-CSF group and 292 patients were treated in the placebo and G-CSF group. Patients received daily morning doses of G-CSF 10 micrograms/kg for 4 days prior to the first dose of Mozobil 0.24 mg/kg SC or placebo and on each morning prior to apheresis. The adverse reactions that occurred in ≥ 5% of the patients who received Mozobil regardless of causality and were more frequent with Mozobil than placebo during HSC mobilization and apheresis are shown in Table 2. 

Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.

In the randomized studies, 34% of patients with NHL or MM had mild to moderate injection site reactions at the site of subcutaneous administration of Mozobil. These included erythema, hematoma, hemorrhage, induration, inflammation, irritation, pain, paresthesia, pruritus, rash, swelling, and urticaria.

Mild to moderate systemic reactions were observed in less than 1% of patients approximately 30 min after Mozobil administration. Events included one or more of the following: urticaria (n = 2), periorbital swelling (n = 2), dyspnea (n = 1) or hypoxia (n = 1). Symptoms generally responded to treatments (e.g., antihistamines, corticosteroids, hydration or supplemental oxygen) or resolved spontaneously.

Vasovagal reactions, orthostatic hypotension, and/or syncope can occur following subcutaneous injections.   In Mozobil oncology and healthy volunteer clinical studies, less than 1% of subjects experienced vasovagal reactions following subcutaneous administration of Mozobil doses ≤ 0.24 mg/kg. The majority of these events occurred within 1 hour of Mozobil administration. Because of the potential for these reactions, appropriate precautions should be taken.

Other adverse reactions in the randomized studies that occurred in < 5% of patients but were reported as related to Mozobil during HSC mobilization and apheresis included abdominal pain, hyperhidrosis, abdominal distention, dry mouth, erythema, stomach discomfort, malaise, hypoesthesia oral, constipation, dyspepsia, and musculoskeletal pain.

Table 2: Adverse Reactions in ≥ 5% of Non-Hodgkin’s Lymphoma and Multiple Myeloma Patients Receiving Mozobil® and More Frequent than Placebo During HSC Mobilization and Apheresis
 Percent of Patients (%)
   Mozobil® and G-CSF
(n = 301)
Placebo and G-CSF
(n = 292)
  All
Grades  Grades based on criteria from the World Health Organization (WHO)  
Grade
3
Grade
4
All
Grades
Grade
3
Grade
4
Gastrointestinal disorders            
    Diarrhea  37 < 1 0 17 0 0
    Nausea 34 1 0 22 0 0
    Vomiting     10 < 1 0 6 0 0
    Flatulence 7 0 0 3 0 0
General disorders and administration site conditions            
    Injection site reactions         34 0 0 10 0 0
    Fatigue  27 0 0 25 0 0
Musculoskeletal and connective tissue disorders                
    Arthralgia  13 0 0 12 0 0
Nervous system disorders            
    Headache 22 < 1 0 21 1 0
    Dizziness 11 0 0 6 0 0
Psychiatric disorders            
   Insomnia 7 0 0 5 0 0

Based on in vitro data, plerixafor is not a substrate, inhibitor or inducer of human cytochrome P450 isozymes. Plerixafor is not likely to be implicated in in vivo drug-drug interactions involving cytochrome P450s. At concentrations similar to what are seen clinically, plerixafor did not act as a substrate or inhibitor of P-glycoprotein in an in vitro study. [see Clinical Pharmacology (12.3)]

Pregnancy Category D Plerixafor was teratogenic in animals. Plerixafor administered to pregnant rats induced embryo-fetal toxicities including fetal death, increased resorptions and post-implantation loss, decreased fetal weights, anophthalmia, shortened digits, cardiac interventricular septal defect, ringed aorta, globular heart, hydrocephaly, dilatation of olfactory ventricles, and retarded skeletal development. Embryo-fetal toxicities occurred mainly at a dose of 90 mg/m (approximately 10 times the recommended human dose of 0.24 mg/kg when compared on a mg/m basis or 10 times the AUC in subjects with normal renal function who received a single dose of 0.24 mg/kg).

It is not known whether plerixafor is excreted in human milk. Because many drugs are excreted in human milk, and because of the potential for serious adverse reactions in nursing infants from Mozobil, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.

The safety and efficacy of Mozobil in pediatric patients have not been established in controlled clinical studies.

Of the total number of subjects in controlled clinical studies of Mozobil, 24% were 65 and over, while 0.8% were 75 and over. No overall differences in safety or effectiveness were observed between these subjects and younger subjects, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out.

Since plerixafor is mainly excreted by the kidney, no dose modifications are necessary in elderly individuals with normal renal function.  In general, care should be taken in dose selection for elderly patients due to the greater frequency of decreased renal function with advanced age.  Dosage adjustment in elderly patients with CL ≤ 50 mL/min is recommended. [see  Dosage and Administration (2.3) and Clinical Pharmacology (12.3) ]

In patients with moderate and severe renal impairment (CL ≤ 50 mL/min), reduce the dose of plerixafor by one-third to 0.16 mg/kg. [see  Dosage and Administration (2.3) and  Clinical Pharmacology (12.3) ]

Based on limited data at doses above the recommended dose of 0.24 mg/kg SC, the frequency of gastrointestinal disorders, vasovagal reactions, orthostatic hypotension, and/or syncope may be higher.

Mozobil (plerixafor injection) is a sterile, preservative-free, clear, colorless to pale yellow, isotonic solution for subcutaneous injection. Each mL of the sterile solution contains 20 mg of plerixafor.  Each single-use vial is filled to deliver 1.2 mL of the sterile solution that contains 24 mg of plerixafor and 5.9 mg of sodium chloride in Water for Injection adjusted to a pH of 6.0 to 7.5 with hydrochloric acid and with sodium hydroxide, if required. 

Plerixafor is a hematopoietic stem cell mobilizer with a chemical name 1, 1'-[1,4-phenylenebis (methylene)]-bis-1,4,8,11- tetraazacyclotetradecane.  It has the molecular formula CHNThe molecular weight of plerixafor is 502.79 g/mol. The structural formula is provided in Figure 1.

Figure 1: Structural Formula

Plerixafor is a white to off-white crystalline solid.  It is hygroscopic. Plerixafor has a typical melting point of 131.5 °C. The partition coefficient of plerixafor between 1-octanol and pH 7 aqueous buffer is < 0.1.

Plerixafor is an inhibitor of the CXCR4 chemokine receptor and blocks binding of its cognate ligand, stromal cell-derived factor-1α (SDF-1α).  SDF-1α and CXCR4 are recognized to play a role in the trafficking and homing of human hematopoietic stem cells (HSCs) to the marrow compartment. Once in the marrow, stem cell CXCR4 can act to help anchor these cells to the marrow matrix, either directly via SDF-1α or through the induction of other adhesion molecules. Treatment with plerixafor resulted in leukocytosis and elevations in circulating hematopoietic progenitor cells in mice, dogs and humans.  CD34+ cells mobilized by plerixafor were capable of engraftment with long-term repopulating capacity up to one year in canine transplantation models.

Data on the fold increase in peripheral blood CD34+ cell count (cells/mcL) by apheresis day were evaluated in two placebo-controlled clinical studies in patients with NHL and MM (Study 1 and Study 2, respectively). The fold increase in CD34+ cell count (cells/mcL) over the 24-hour period starting from the day prior to the first apheresis and ending the next morning just before the first apheresis is summarized in Table 3.  During this 24-hour period, a single dose of Mozobil or placebo was administered 10 to 11 hours prior to apheresis.

In pharmacodynamic studies of Mozobil in healthy volunteers, peak mobilization of CD34+ cells was observed between 6 and 9 hours after administration. In pharmacodynamic studies of Mozobil in conjunction with G-CSF in healthy volunteers, a sustained elevation in the peripheral blood CD34+ count was observed from 4 to 18 hours after plerixafor administration with a peak CD34+ count between 10 and 14 hours.

Table 3: Fold Increase in Peripheral Blood CD34+ Cell Count Following Pretreatment with G-CSF and Administration of Plerixafor
 
 Study
Mozobil® and G-CSF Placebo and G-CSF
   Median  Mean (SD)   Median    Mean (SD)
 Study 1  5.0  6.1 (5.4)  1.4  1.9 (1.5)
 Study 2  4.8  6.4 (6.8)  1.7  2.4 (7.3)

The single-dose pharmacokinetics of plerixafor 0.24 mg/kg were evaluated in patients with NHL and MM following pre-treatment with G-CSF (10 micrograms/kg once daily for 4 consecutive days).  Plerixafor exhibits linear kinetics between the 0.04 mg/kg to 0.24 mg/kg dose range.  The pharmacokinetics of plerixafor were similar across clinical studies in healthy subjects who received plerixafor alone and NHL and MM patients who received plerixafor in combination with G-CSF.

A population pharmacokinetic analysis incorporated plerixafor data from 63 subjects (NHL patients, MM patients, subjects with varying degrees of renal impairment, and healthy subjects) who received a single SC dose (0.04 mg/kg to 0.24 mg/kg) of plerixafor.  A two-compartment disposition model with first order absorption and elimination was found to adequately describe the plerixafor concentration-time profile. Significant relationships between clearance and creatinine clearance (CL), as well as between central volume of distribution and body weight were observed.  The distribution half-life (t) was estimated to be 0.3 hours and the terminal population half-life (t) was 5.3 hours in patients with normal renal function.

The population pharmacokinetic analysis showed that the mg/kg-based dosage results in an increased plerixafor exposure (AUC) with increasing body weight.  There is limited experience with the 0.24 mg/kg dose of plerixafor in patients weighing above 160 kg.  Therefore the dose should not exceed that of a 160 kg patient (i.e., 40 mg/day if CL is > 50 mL/min and 27 mg/day if CL is ≤ 50 mL/min).  [see Dosage and Administration (2.1 ,  2.3) ]

Absorption Peak plasma concentrations occurred at approximately 30 - 60 minutes after a SC dose.

Distribution Plerixafor is bound to human plasma proteins up to 58%. The apparent volume of distribution of plerixafor in humans is 0.3 L/kg demonstrating that plerixafor is largely confined to, but not limited to, the extravascular fluid space.

Metabolism The metabolism of plerixafor was evaluated with in vitro assays.  Plerixafor is not metabolized as shown in assays using human liver microsomes or human primary hepatocytes and does not exhibit inhibitory activity in vitro towards the major drug metabolizing cytochrome P450 enzymes (1A2, 2C9, 2C19, 2D6, and 3A4/5). In in vitro studies with human hepatocytes, plerixafor does not induce CYP1A2, CYP2B6, or CYP3A4 enzymes. These findings suggest that plerixafor has a low potential for involvement in cytochrome P450-dependent drug-drug interactions.

Elimination The major route of elimination of plerixafor is urinary. Following a 0.24 mg/kg dose in healthy volunteers with normal renal function, approximately 70% of the dose was excreted in the urine as the parent drug during the first 24 hours following administration. In studies with healthy subjects and patients, the terminal half-life in plasma ranges between 3 and 5 hours. At concentrations similar to what are seen clinically, plerixafor did not act as a substrate or inhibitor of P-glycoprotein in an in vitro study with MDCKII and MDCKII-MDR1 cell models.

Renal Impairment Following a single 0.24 mg/kg SC dose, plerixafor clearance was reduced in subjects with varying degrees of renal impairment and was positively correlated with CL.  The mean AUCof plerixafor in subjects with mild (CL 51-80 mL/min), moderate (CL 31-50 mL/min), and severe (CL < 31 mL/min) renal impairment was 7%, 32%, and 39% higher than healthy subjects with normal renal function, respectively.  Renal impairment had no effect on C. A population pharmacokinetic analysis indicated an increased exposure (AUC)in patients with moderate and severe renal impairment compared to patients with CL > 50 mL/min. These results support a dose reduction of one-third in patients with moderate to severe renal impairment (CL ≤ 50 mL/min) in order to match the exposure in patients with normal renal function. The population pharmacokinetic analysis showed that the mg/kg-based dosage results in an increased plerixafor exposure (AUC) with increasing body weight; therefore if CL is ≤ 50 mL/min the dose should not exceed 27 mg/day.  [see  Dosage and Administration (2.3) ]

Since plerixafor is primarily eliminated by the kidneys, coadministration of plerixafor with drugs that reduce renal function or compete for active tubular secretion may increase serum concentrations of plerixafor or the coadministered drug.  The effects of coadministration of plerixafor with other drugs that are renally eliminated or are known to affect renal function have not been evaluated.

Race Clinical data show similar plerixafor pharmacokinetics for Caucasians and African-Americans, and the effect of other racial/ethnic groups has not been studied. 

Gender Clinical data show no effect of gender on plerixafor pharmacokinetics.

Age Clinical data show no effect of age on plerixafor pharmacokinetics.

There is no indication of a QT/QTc prolonging effect of Mozobil in single doses up to 0.40 mg/kg. In a randomized, double-blind, crossover study, 48 healthy subjects were administered a single subcutaneous dose of Mozobil (0.24 mg/kg and 0.40 mg/kg) and placebo. Peak concentrations for 0.40 mg/kg Mozobil were approximately 1.8-fold higher than the peak concentrations following the 0.24 mg/kg single subcutaneous dose.

Carcinogenicity studies with plerixafor have not been conducted.

Plerixafor was not genotoxic in an in vitro bacterial mutation assay (Ames test in Salmonella ), an in vitro chromosomal aberration test using V79 Chinese hamster cells, or an in vivo bone marrow micronucleus test in rats after subcutaneous doses up to 25 mg/kg (150 mg/m).

The effect of plerixafor on human fertility is unknown.  The effect of plerixafor on male or female fertility was not studied in designated reproductive toxicology studies.  The staging of spermatogenesis measured in a 28-day repeated dose toxicity study in rats revealed no abnormalities considered to be related to plerixafor.  No histopathological evidence of toxicity to male or female reproductive organs was observed in 28-day repeated dose toxicity studies.

The efficacy and safety of Mozobil in conjunction with G-CSF in non-Hodgkin’s lymphoma (NHL) and multiple myeloma (MM) were evaluated in two placebo-controlled studies (Studies 1 and 2).  Patients were randomized to receive either Mozobil 0.24 mg/kg or placebo on each evening prior to apheresis. Patients received daily morning doses of G-CSF 10 micrograms/kg for 4 days prior to the first dose of Mozobil or placebo and on each morning prior to apheresis. Two hundred and ninety-eight (298) NHL patients were included in the primary efficacy analyses for Study 1. The mean age was 55.1 years (range 29-75) and 57.5 years (range 22-75) in the Mozobil and placebo groups, respectively, and 93% of subjects were Caucasian. Three hundred and two (302) MM patients were included in the primary efficacy analyses for Study 2. The mean age was 58.2 years (range 28-75) and 58.5 years (range 28-75) in the Mozobil and placebo groups, respectively, and 81% of subjects were Caucasian.

In Study 1, 59% of NHL patients who were mobilized with Mozobil and G-CSF collected ≥ 5 X 10 CD34+ cells/kg from the peripheral blood in four or fewer apheresis sessions, compared with 20% of patients who were mobilized with placebo and G-CSF (p < 0.001). Other CD34+ cell mobilization outcomes showed similar findings (Table 4). 

The median number of days to reach ≥ 5 x 10 CD34+ cells/kg was 3 days for the Mozobil group and not evaluable for the placebo group. Table 5 presents the proportion of patients who achieved ≥ 5 x 10 CD34+ cells/kg by apheresis day.

In Study 2, 72% of MM patients who were mobilized with Mozobil and G-CSF collected ≥ 6 X 10 CD34+ cells/kg from the peripheral blood in two or fewer apheresis sessions, compared with 34% of patients who were mobilized with placebo and G-CSF (p < 0.001). Other CD34+ cell mobilization outcomes showed similar findings (Table 6). 

The median number of days to reach ≥ 6 x 10 CD34+ cells/kg was 1 day for the Mozobil group and 4 days for the placebo group. Table 7 presents the proportion of patients who achieved ≥ 6 x 10 CD34+ cells/kg by apheresis day.

Multiple factors can influence time to engraftment and graft durability following stem cell transplantation. For transplanted patients in the Phase 3 studies, time to neutrophil and platelet engraftment and graft durability were similar across the treatment groups.

Table 4: Study 1 Efficacy Results - CD34+ Cell Mobilization in NHL Patients
 Efficacy Endpoint Mozobil® and
G-CSF
(n = 150)
Placebo and
G-CSF
(n = 148)
p-value  p-value calculated using Pearson's Chi-Squared test  
Patients achieving ≥ 5 X 106 cells/kg in ≤ 4 apheresis days 89 (59%) 29 (20%) < 0.001
Patients achieving ≥ 2 X 106 cells/kg in ≤ 4 apheresis days 130 (87%) 70 (47%) < 0.001
Table 5: Study 1 Efficacy Results - Proportion of Patients Who Achieved ≥ 5 x 106 CD34+ cells/kg by Apheresis Day in NHL Patients
Days Proportion   Percents determined by Kaplan Meier method   
in Mozobil® and G-CSF
(n=147   n includes all patients who received at least one day of apheresis )
 Proportion  
in Placebo and G-CSF
(n = 142)
1 27.9% 4.2%
2 4

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Genzyme Corporation

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Clinical Trials [8 Associated Clinical Trials listed on BioPortfolio]

Mozobil for Autologous Stem Cell Mobilization

The aim of this study is to evaluate Plerixafor (MOZOBIL) plus recombinant human G-CSF (G-CSF) efficiency in mobilizing sufficient number of stem cells from Lymphoma (NHL and HL) patients ...

Clinical Phase II Trial to Evaluate CD34+ Cells Mobilization and Collection in Patients With Fanconi Anemia for Subsequent Transduction With a Lentiviral Vector Carring FANCA Gene. FANCOSTEM-1

Fanconi anemia (FA) is a congenital disease characterized by bone marrow failure and increased incidence of malignant tumors. The Project pursue the optimization of the collection of hemat...

Combination of Ibuprofen, G-CSF and Plerixafor as Stem Cells Mobilization Regimen in Patients Affected by X-CGD

This is a phase II exploratory study conducted to evaluate the safety and efficacy of the combination of Ibuprofen, G-CSF and Plerixafor as stem cell mobilization regimen in patients affec...

Exploratory Trial to Estimate Proportion of Patients With Tumor Cell Contaminated Leukapheresis Products With and Without Bortezomib With In-vivo Purging - Multiple Myeloma (MM)

Explore stem cell collection with or without bortezomib with in-vivo purging in multiple myeloma.

Feasibility and Efficiency Study of Leukemic Cell Mobilization With Plerixafor Injection

The study will be conducted as a single center Phase I/II study to evaluate the safety of administering Plerixafor administered as part of a myeloablative preparative regimen (Institutiona...

PubMed Articles [0 Results]

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