Infusion-related reactions:   Infusion-related deaths (death within 24 hours of infusion) have been reported at a rate of approximately 0.04-0.07% (4-7 per 10,000 patients treated). These events appear as manifestations of an infusion-related complex and include hypoxia, pulmonary infiltrates, adult respiratory distress syndrome, myocardial infarction, ventricular fibrillation or cardiogenic shock. Nearly all fatal infusion-related events occurred in association with the first infusion. In the reported cases, the following factors were more frequently associated with fatal outcomes: women, patients with pulmonary infiltrates, and patients with CLL or mantle cell lymphoma (see ).

Regarding the management of infusion-related reactions:

Tumor Lysis Syndrome (TLS):   Acute renal failure requiring dialysis with instances of fatal outcome has been reported in the setting of TLS. Assessment of serum electrolytes and renal function is indicated in patients with rapid decreases in tumor volume (see ).

The RITUXAN (Rituximab) antibody is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG 1 kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences. Rituximab is composed of two heavy chains of 451 amino acids and two light chains of 213 amino acids (based on cDNA analysis) and has an approximate molecular weight of 145 kD. Rituximab has a binding affinity for the CD20 antigen of approximately 8.0 nM.

The chimeric anti-CD20 antibody is produced by mammalian cell (Chinese Hamster Ovary) suspension culture in a nutrient medium containing the antibiotic gentamicin. Gentamicin is not detectable in the final product. The anti-CD20 antibody is purified by affinity and ion exchange chromatography. The purification process includes specific viral inactivation and removal procedures. Rituximab drug product is manufactured from either bulk drug substance manufactured by Genentech, Inc. (US License No. 1048), or utilizing formulation bulk Rituximab supplied by IDEC Pharmaceuticals Corporation (US License No. 1235) under a shared manufacturing arrangement.

RITUXAN is a sterile, clear, colorless, preservative-free liquid concentrate for intravenous (IV) administration. RITUXAN is supplied at a concentration of 10 mg/mL in either 100 mg (10 mL) or 500 mg (50 mL) single-use vials. The product is formulated for IV administration in 9.0 mg/mL sodium chloride, 7.35 mg/mL sodium citrate dihydrate, 0.7 mg/mL polysorbate 80, and Sterile Water for Injection. The pH is adjusted to 6.5.


Rituximab binds specifically to the antigen CD20 (human B-lymphocyte-restricted differentiation antigen, Bp35), a hydrophobic transmembrane protein with a molecular weight of approximately 35 kD located on pre-B and mature B lympocytes. 1,2 The antigen is also expressed on >90% of B-cell non-Hodgkin' lymphomas (NHL) 3 but is not found on hematopoietic stem cells, pro-B cells, normal plasma cells or other normal tissues. 4 CD20 regulates an early step(s) in the activation process for cell cycle initiation and differentiation, 4 and possibly functions as a calcium ion channel. 5 CD20 is not shed from the cell surface and does not internalize upon antibody binding. 6 Free CD20 antigen is not found in the circulation. 2

Pre and Toxicology

Mechanism of Action: The Fab domain of Rituximab binds to thd CD20 antigen on B lymphocytes, and the Fc domain recruits immune effector functions to mediate B-cell lysis in vitro. Possible mechanisms of cell lysis include complement-dependent cytotoxicity (CDC) 7 and antibody-dependent cell mediated cytotoxicity (ADCC). The antibody has been shown to induce apoptosis in the DHL-4 human B-cell lymphoma line. 8

Normal Tissue Cross-reactivity: Rituximab binding was observed on lymphoid cells in the thymus, the white pulp of the spleen, and a majority of B lymphocytes in peripheral blood and lymph nodes. Little or no binding was observed in the non-lymphoid tissues examined.

Human /Pharmacodynamics

In patients given single doses at 10, 50, 100, 250 or 500 mg/m 2 as an IV infusion, serum levels and the half-life of Rituximab were proportional to dose. In nine patients given 375 mg/m 2 as an IV infusion for four doses, the mean serum half-life was 59.8 hours (range 11.1 to 104.6 hours) after the first infusion and 174 hours (range 26 to 442 hours) after the fourth infusion. The wide range of half-lives may reflect the variable tumor burden among patients and the changes in CD20 positive (normal and malignant) B-cell populations upon repeated administrations.

Rituximab at a dose of 375 mg/m 2 was administered as an IV infusion at weekly intervals for four doses to 166 patients. The peak and trough serum levels of Rituximab were inversely correlated with baseline values for the number of circulating CD20 positive B cells and measures of disease burden. Median steady-state serum levels were higher for responders compared to nonresponders; however, no difference was found in the rate of elimination as measured by serum half-life. Serum levels were higher in patients with International Working Formulation (IWF) subtypes B, C, and D as compared to those with subtype A. Rituximab was detectable in the serum of patients three to six months after completion of treatment.

The pharmacokinetic profile of Rituximab when administered as six infusions of 375 mg/m 2 in combination with six cycles of CHOP chemotherapy was similar to that seen with Rituximab alone.

Administration of RITUXAN resulted in a rapid and sustained depletion of circulating and tissue-based B cells. Lymph node biopsies performed 14 days after therapy showed a decrease in the percentage of B cells in seven of eight patients who had received single doses of Rituximab >/=100 mg/m 2 . 9 Among the 166 patients in the pivotal study, circulating B cells (measured as CD19 positive cells) were depleted within the first three doses with sustained depletion for up to 6 to 9 months posttreatment in 83% of patients. One of the responding patients (1%), failed to show significant depletion of CD19 positive cells after the third infusion of Rituximab as compared to 19% of the nonresponding patients. B-cell recovery began at approximately six months following completion of treatment. Median B-cell levels returned to normal by twelve months following completion of treatment.

There were sustained and statistically significant reductions in both IgM and IgG serum levels observed from 5 through 11 months following Rituximab administration. However, only 14% of patients had reductions in IgM and/or IgG serum levels, resulting in values below the normal range.


A multicenter, open-label, single-arm study was conducted in 166 patients with relapsed or refractory low-grade or follicular B-cell NHL who received 375 mg/m 2 of RITUXAN given as an IV infusion weekly for four doses. Patients with tumor masses >10 cm or with >5,000 lymphocytes/µL in the peripheral blood were excluded from the study. The overall response rate (ORR) was 48% (80/166) with a 6% (10/166) complete response (CR) and a 42% (70/166) partial response (PR) rate. Disease-related signs and symptoms (including B-symptoms) were present in 23% (39/166) of patients at study entry and resolved in 64% (25/39) of those patients. The median time to onset of response was 50 days and the median duration of response is projected to be 10 to 12 months.

In a multivariate analysis, the ORR was higher in patients with IWF B, C, and D histologic subtypes as compared to IWF subtype A (58% vs. 12%), higher in patients whose largest lesion was <5 cm vs. >7 cm in greatest diameter (53% vs. 38%), and higher in patients with chemosensitive relapse as compared to chemoresistant (defined as duration of response <3 months) relapse (53% vs. 36%). ORR in patients previously treated with autologous bone marrow transplant was 78% (18/23). The following factors were not associated with a lower response rate: age >/=60 years, extranodal disease, prior anthracycline therapy, and bone marrow involvement.

In a second multicenter, multiple-dose study, 37 patients with relapsed or refractory B-cell NHL received 375 mg/m 2 of RITUXAN as an IV infusion once weekly for four doses. 10,11 The ORR was 46% with a median duration of response of 8.6 months (range 2.6 to 26.2+). Single doses of up to 500 mg/m 2 were well tolerated. 9

Twenty patients have received two courses and one patient has received three courses of RITUXAN as four weekly infusions of 375 mg/m 2 per infusion. The percentage of patients reporting adverse events upon retreatment was similar to that reported following the first course, although the incidence of specific adverse events differed (see ADVERSE REACTIONS ). All patients had obtained an objective clinical response (CR or PR) to the first course of RITUXAN; upon retreatment, 6 of 12 patients evaluable for response obtained a complete or partial remission.

Twenty-nine patients with relapsed or refractory, bulky (single lesion of >10 cm in diameter), low-grade NHL received 375 mg/m 2 of RITUXAN as four weekly infusions. The overall incidence of adverse events and the incidence of Grade 3 and 4 adverse events was higher in patients with bulky disease than in patients with non-bulky disease (see ADVERSE REACTIONS ). Ten of 21 patients evaluable for response have obtained a complete or partial remission.

RITUXAN is indicated for the treatment of patients with relapsed or refractory low-grade or follicular, CD20 positive, B-cell non-Hodgkin' lymphoma.


RITUXAN is contraindicated in patients with known Type I hypersensitivity or anaphylactic reactions to murine proteins or to any component of this product. (See .)

   (see BOXED )

Infusion-Related Events (see BOXED WARNING ):   An infusion-related symptom complex consisting of fever and chills/rigors occurred in the majority of patients during the first RITUXAN infusion. Other frequent infusion-related symptoms included nausea, urticaria, fatigue, headache, pruritus, bronchospasm, dyspnea, sensation of tongue or throat swelling (angioedema), rhinitis, vomiting, hypotension, flushing, and pain at disease sites. These reactions generally occurred within 30 minutes to 2 hours of beginning the first infusion, and resolved with slowing or interruption of the RITUXAN infusion and with supportive care (diphenhydramine, acetaminophen, IV saline, and vasopressors). RITUXAN infusion should be interrupted for severe reactions. In most cases, the infusion can be resumed at a 50% reduction in rate (e.g., from 100 mg/hr to 50 mg/hr) when symptoms have completely resolved. In clinical studies, the incidence of infusion-related events decreased from 80% (7% Grade 3/4) during the first infusion to approximately 40% (5% to 10% Grade 3/4) with subsequent infusions. Mild to moderate hypotension requiring interruption of RITUXAN infusion with or without the administration of IV saline occurred in 32 (10%) patients. Angioedema was reported in 41 (13%) patients and was serious in one patient. Bronchospasm occurred in 24 (8%) patients; one-quarter of these patients were treated with bronchodilators.

Tumor Lysis Syndrome (see BOXED WARNING ):   TLS, characterized by rapid reduction in tumor volume, renal insufficiency, hyperkalemia, hypocalcemia, hyperuricemia, or hyperphosphatasemia, has been reported within 12 to 24 hours after the first RITUXAN infusion at a reported rate of 0.04%-0.05%. The risks of TLS appear to be higher in patients with high numbers of circulating malignant cells. Correction of electrolytes abnormalities, monitoring of renal function and fluid balance, and supportive care, including dialysis, should be initiated as indicated. Following complete resolution of the complications of TLS, RITUXAN has been tolerated when re-administered in conjunction with prophylactic therapy for TLS in a limited number of cases.


RITUXAN is associated with hypersensitivity reactions which may respond to adjustments in the infusion rate. Hypotension, bronchospasm, and angioedema have occurred in association with RITUXAN infusion as part of an infusion-related symptom complex. RITUXAN infusion should be interrupted for severe reactions and can be resumed at a 50% reduction in rate (e.g., from 100 mg/hr to 50 mg/hr) when symptoms have completely resolved. Treatment of these symptoms with diphenhydramine and acetaminophen is recommended; additional treatment with bronchodilators or IV saline may be indicated. In most cases, patients who have experienced non-life-threatening reactions have been able to complete the full course of therapy. (See DOSAGE and ADMINISTRATION .) Medications for the treatment of hypersensitivity reactions, e.g., epinephrine, antihistamines and corticosteroids, should be available for immediate use in the event of a reaction during administration.


Infusions should be discontinued in the event of serious or life-threatening cardiac arrhythmias. Patients who develop clinically significant arrhythmias should undergo cardiac monitoring during and after subsequent infusions of RITUXAN. Patients with preexisting cardiac conditions including arrhythmias and angina have had recurrences of these events during RITUXAN therapy and should be monitored throughout the infusion and immediate post-infusion period.


Laboratory Monitoring:   Complete blood counts (CBC) and platelet counts should be obtained at regular intervals during RITUXAN therapy and more frequently in patients who develop cytopenias (see ADVERSE REACTIONS ).

Drug/Laboratory Interactions:   There have been no formal drug interaction studies performed with RITUXAN.

HAMA/HACA Formation:   Human anti-murine antibody (HAMA) was not detected in 67 patients evaluated. Less than 1.0% (3/355) of patients evaluated for human anti-chimeric antibody (HACA) were positive. Patients who develop HAMA/HACA titers may have allergic or hypersensitivity reactions when treated with this or other murine or chimeric monoclonal antibodies.

Immunization   The safety of immunization with any vaccine, particularly live viral vaccines, following RITUXAN therapy has not been studied. The ability to generate a primary or anamnestic humoral response to any vaccine has also not been studied.

Carcinogenesis, Mutagenesis, Impairment of Fertility:   No long-term animal studies have been performed to establish the carcinogenic or mutagenic potential of RITUXAN, or to determine its effects on fertility in males or females. Individuals of childbearing potential should use effective contraceptive methods during treatment and for up to 12 months following RITUXAN therapy.

Pregnancy Category C:   Animal reproduction studies have not been conducted with RITUXAN. It is not known whether RITUXAN can cause fetal harm when administered to a pregnant woman or whether it can affect reproductive capacity. Human IgG is known to pass the placental barrier, and thus may potentially cause fetal B-cell depletion; therefore, RITUXAN should be given to a pregnant woman only if clearly needed.

Nursing Mothers:   It is not known whether RITUXAN is excreted in human milk. Because human IgG is excreted in human milk and the potential for absorption and immunosuppression in the infant is unknown, women should be advised to discontinue nursing until circulating drug levels are no longer detectable. (See .)

Pediatric Use:   The safety and effectiveness of RITUXAN in pediatric patients have not been established.


Safety data, except where indicated, are based on 315 patients treated in five single-agent studies of RITUXAN. These include patients with bulky disease (lesions >10 cm), those who have received more than one course of RITUXAN, and patients receiving 375 mg/m 2 for eight doses.

Infusion-Related Events:    (See BOXED WARNING and .)

Immunologic Events:   RITUXAN induced B-cell depletion in 70 to 80% of patients was associated with decreased serum immunoglobulins in a minority of patients. The incidence of infection did not appear to be increased. During the treatment period, 50 out of 166 patients (30%) in the pivotal trial developed 68 infectious events; six (9%) were Grade 3 in severity and none were Grade 4 events. Of the six serious infections events, none were associated with neutropenia. The serious bacterial events included sepsis due to Listeria (n=1), Staphylococcal bacteremia (n=1), and polymicrobial sepsis (n=1). In the posttreatment period (30 days to 11 months following the last dose), bacterial infections included sepsis (n=1); significant viral infections included Herpes simplex infections (n=2) and Herpes zoster (n=3). Additional reports of focal bacterial infections, sepsis, and viral infections have been received in the postmarketing setting. Serious infections, including sepsis, have been reported in patients with and without neutropenia.

Retreatment Events:   Twenty-one patients have received more than one course of RITUXAN. The percentage of patients reporting any adverse event upon retreatment was similar to the percentage of patients reporting adverse events upon initial exposure. The following adverse events were reported more frequently in retreated subjects: asthenia, throat irritation, flushing, tachycardia, anorexia, leukopenia, thrombocytopenia, anemia, peripheral edema, dizziness, depression, respiratory symptoms, night sweats, and pruritus.

Hematologic Events:   Severe cytopenias were reported including thrombocytopenia (1.3%), neutropenia (1.9%), and anemia (1.0%). A single occurrence of transient aplastic anemia (pure red cell aplasia) and two occurrences of hemolytic anemia following RITUXAN therapy were reported. In addition, there have been rare postmarketing reports of prolonged pancytopenia and marrow hypoplasia.

Cardiac Events (see BOXED WARNING ):   Four patients developed ventricular or supraventricular arrhythmias and one patient developed angina in association with the RITUXAN infusion. Rare, fatal cardiac failure with symptomatic onset weeks after RITUXAN has also been reported. Patients who develop clinically significant cardiopulmonary events should have RITUXAN infusion discontinued.

Pulmonary Events (see BOXED WARNING ):   Three pulmonary events have been reported in temporal association with RITUXAN infusion as a single agent: acute, infusion-related bronchospasm, an acute pneumonitis presenting 1-4 weeks post-RITUXAN infusion, and bronchiolitis obliterans. The bronchiolitis obliterans was associated with progressive pulmonary symptoms and culminated in death several months following the last RITUXAN infusion. The safety of resumption or continued administration of RITUXAN in patients with pneumonitis or bronchiolitis obliterans is unknown.

Table 1
Adverse Events >/=5% of Patients (N=315)
All Grades
Any Adverse Event
Body As A Whole
154 49
102 32
49 16
43 14
 Throat Irritation
19 6
 Abdominal Pain
18 6
32 10
55 18
23 7
33 11
25 8
21 7
Metabolic and Nutritional System
41 13
Musculo-Skeletal System
21 7
23 7
25 8
24 8
Skin and Appendages
32 10
31 10
24 8

Severe and life-threatening (Grade 3 and 4) events were reported in 10% (32/315) of patients. The following Grade 3 and 4 adverse events were reported: neutropenia (1.9%), chills (1.6%), leukopenia and thrombocytopenia (1.3% for each), hypotension, anemia, bronchospasm, and urticaria (1.0% for each), headache, abdominal pain, and arrhythmia (0.6% for each), asthenia, hypertension, nausea, vomiting, coagulation disorder, angioedema, arthralgia, pain, rhinitis, increased cough, dyspnea, bronchiolitis obliterans, hypoxia, asthma, pruritus, and rash (one patient each, 0.3%).

The following adverse events occurred in >/=1.0% but <5.0% of patients, in order of decreasing incidence: flushing, arthralgia, diarrhea, anemia, cough increase, hypertension, lacrimation disorder, pain, hyperglycemia, back pain, peripheral edema, paresthesia, dyspepsia, chest pain, anorexia, anxiety, malaise, tachycardia, agitation, insomnia, sinusitis, conjunctivitis, abdominal enlargement, postural hypotension, LDH increase, hypocalcemia, hypesthesia, respiratory disorder, tumor pain, pain at injection site, bradycardia, hypertonia, nervousness, bronchitis, and taste perversion.

Multisystem adverse events--The following serious adverse reactions have been reported at a frequency of less than 0.1% in the postmarketing setting:

Body as a Whole: Lupus-like syndrome and serum sickness

Cardiovascular System: Systemic vasculitis

Musculoskeletal System: Polyarticular arthritis

Respiratory System: Pleuritis

Skin and Appendages: Severe bullous skin reactions (including toxic epidermal necrolysis) and pemphigus; some with fatal outcome

Special Senses: Optic neuritis and uveitis

Several of these events were reported as individual components of multisystem processes (e.g., optic neuritis in a patient with systemic vasculitis, pleuritis in association with lupus-like syndrome, etc.) and often in conjunction with rash and polyarthritis.

The proportion of patients reporting any adverse event was similar in patients with bulky disease and those with lesions <10 cm in diameter. However, the incidence of dizziness, neutropenia, thrombocytopenia, myalgia, anemia, and chest pain was higher in patients with lesions >10 cm. The incidence of any Grade 3 and 4 event was higher (31% vs. 13%) and the incidence of Grade 3 or 4 neutropenia, anemia, hypotension, and dyspnea was also higher in patients with bulky disease compared with patients with lesions <10 cm.


There has been no experience with overdosage in human clinical trials. Single doses higher than 500 mg/m 2 have not been tested.


Usual Dose:

The recommended dosage of RITUXAN is 375 mg/m 2 given as an IV infusion once weekly for four doses (Days 1, 8, 15, and 22). RITUXAN may be administered in an outpatient setting. DO NOT ADMINISTER AS AN INTRAVENOUS PUSH OR BOLUS. (See Administration ).

Instructions for Administration

Preparation for Administration:   Use appropriate aseptic technique. Withdraw the necessary amount of RITUXAN and dilute to a final concentration of 1 to 4 mg/mL into an infusion bag containing either 0.9% Sodium Chloride, USP, or 5% Dextrose in Water, USP. Gently invert the bag to mix the solution. Discard any unused portion left in the vial. Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration.

RITUXAN solutions for infusion are stable at 2-8°C (36-46°F) for 24 hours and at room temperature for an additional 12 hours. No incompatibilities between RITUXAN and polyvinylchloride or polyethylene bags have been observed.

Administration:    DO NOT ADMINISTER AS AN INTRAVENOUS PUSH OR BOLUS. Hypersensitivity reactions may occur (see ). Premedication consisting of acetaminophen and diphenhydramine should be considered before each infusion of RITUXAN. Premedication may attenuate infusion-related events. Since transient hypotension may occur during RITUXAN infusion, consideration should be given to withholding antihypertensive medications 12 hours prior to RITUXAN infusion.

First Infusion: The RITUXAN solution for infusion should be administered intravenously at an initial rate of 50 mg/hr. RITUXAN should not be mixed or diluted with other drugs. If hypersensitivity or infusion-related events do not occur, escalate the infusion rate in 50 mg/hr increments every 30 minutes, to a maximum of 400 mg/hr. If hypersensitivity or an infusion-related event develops, the infusion should be temporarily slowed or interrupted (see ). The infusion can continue at one-half the previous rate upon improvement of patient symptoms.

Subsequent Infusions: Subsequent RITUXAN infusions can be administered at an initial rate of 100 mg/hr, and increased by 100 mg/hr increments at 30-minute intervals, to a maximum of 400 mg/hr as tolerated.

Stability and Storage:   RITXUAN vials are stable at 2-8°C (36-46°F). Do not use beyond expiration date stamped on carton. RITUXAN vials should be protected from direct sunlight.


RITUXAN is supplied as 100 mg and 500 mg of sterile, preservative-free, single-use vials.

Single unit 100 mg carton: Contains one 10 mL vial of RITUXAN (10 mg/mL).

NDC 50242-051-21

Single unit 500 mg carton: Contains one 50 mL vial of RITUXAN (10 mg/mL).

NDC 50242-053-06


NOTE: These photos can be used only for identification by shape, color, and imprint. They do not depict actual or relative size.

The product samples shown here have been supplied by the manufacturer and reproduced in full color by PDR as a quick-reference identification aid. While every effort has been made to assure accurate reproduction, please remember that any visual identification should be considered preliminary. In cases of poisoning or suspected overdosage, the drug' identity should be verified by chemical analysis.



  1. Valentine MA, Meier KE, Rossie S, et al. Phosphorylation of the CD20 phosphoprotein in resting B lymphocytes. J Biol Chem 1989 264(19): 11282-11287.
  2. Einfeld DA, Brown JP, Valentine MA, et al. Molecular cloning of the human B cell CD20 receptor predicts a hydrophobic protein with multiple transmembrane domains. EMBO J 1988 7(3):711-717.
  3. Anderson KC, Bates MP, Slaughenhoupt BL, et al. Expression of human B cell-associated antigens on leukemias and lymphomas: A model of human B cell differentiation. Blood 1984 63(6):1424-1433.
  4. Tedder TF, Boyd AW, Freedman AS, et al. The B cell surface molecule B1 is functionally linked with B cell activation and differentiation. J Immunol 1985 135(2):973-979.
  5. Tedder TF, Zhou LJ, Bell PD, et al. The CD20 surface molecule of B lympocytes functions as a calcium channel. J Cell Biochem 1990 14D:195.
  6. Press OW, Applebaum F, Ledbetter JA, Martin PJ, Zarling J, Kidd P, et al. Monoclonal antibody 1F5 (anti-CD20) serotherapy of human B-cell lymphomas. Blood 1987 69(2):584-591.
  7. Reff ME, Carner C, Chambers KS, Chinn PC, Leonard JE, Raab R, et al. Depletion of B cells in vivo by a chimeric mouse human monoclonal antibody to CD20. Blood 1994 83(2):435-445.
  8. Demidem A, Lam T, Alas S, Hariharan K, Hanna N, and Bonavida B. Chimeric anti-CD20 (IDEC-C2B8) monoclonal antibody sensitizes a B cell lymphoma cell line to cell killing by cytotoxic drugs. Cancer Biotherapy & Radiopharmaceuticals 1997 12(3):177-186.
  9. Maloney DG, Liles TM, Czerwinski C, Waldichuk J, Rosenberg J, Grillo-López A, et al. Phase I clinical trial using escalating single-dose infusion of chimeric anti-CD20 monoclonal antibody (IDEC-C2B8) in patients with recurrent B-cell lymphoma. Blood 1994 84(8):2457-2466.
  10. Maloney DG, Grillo-López AJ, Bodkin D, White CA, Liles T-M, Royston I, et al. IDEC-C2B8: Results of a phase I multiple-dose trial in patients with relapsed non-Hodgkin' lympoma. J Clin Oncol 1997 15(10):3266-3274.
  11. Maloney DG, Grillo-López AJ, White CA, Bodkin D, Schlider RJ, Neidhart JA, et al. IDEC-C2B8 (Rituximab) anti-CD20 monoclonal antibody therapy in patients with relapsed low-grade non-Hodgkin' lymphoma. Blood 1997 90(6):2188-2195.

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