Rituximab

Specification

• Cat#: THA-0014
• Product Name: Rituximab
• Description: Rituximab is a monoclonal anti-CD20 antibody used to treat non-Hodgkin's lymphoma, chronic lymphocytic leukemia, Wegener's granulomatosis, pemphigus vulgaris, and rheumatoid arthritis.
• Sequences: Rituximab heavy chain chimeric: QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK Rituximab light chain chimeric: QIVLSQSPAILSASPGEKVTMTCRASSSVSYIHWFQQKPGSSPKPWIYATSNLASGVPVRFSGSGSGTSYSLTISRVEAEDAATYYCQQWTSNPPTFGGGTKLEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC
• Molecular Weight: 143859.7 Da
• Introduction: Rituximab 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 IgG1 kappa immunoglobulin containing murine light and heavy-chain variable region sequences and human constant region sequences. It was originally approved by the U.S. FDA in 1997 as a single agent to treat patients with B-cell Non-Hodgkin's Lymphoma (NHL), however, has now been approved for a variety of conditions. On November 28, 2018, the US FDA approved Truxima, the first biosimilar to Rituxan (Rituximab).
• Purity: >99% by SDS-Page and HPLC analysis
• Formula: C6416H9874N1688O1987S44
• Appearance: Liquid
• Endotoxin Level: < 0.001 EU/μg of the protein by the LAL method

Pharmaceutical Information

• Pharmacodynamics: Rituximab is a chimeric murine/human monoclonal antibody that binds to the CD20 antigen. CD20 is predominantly expressed on the surface of pre-B and mature B-lymphocytes, allowing rituximab to target and promote lysis in this specific type of cells. In Non-Hodgkin's Lymphoma patients, rituximab treatment depleted circulating and tissue-based B-cells. In a study that included 166 patients, CD19-positive B-cells were depleted within three weeks, and in 83% of patients, cell depletion lasted up to 6-9 months. B-cell levels started to recover at approximately 6 months and returned to normal 12 months after treatment was completed. Approximately 14% of Non-Hodgkin's Lymphoma patients had IgM or IgG serum levels below the normal range. Most rheumatoid arthritis (RA) patients treated with rituximab showed a near-complete depletion of peripheral B lymphocytes within 2 weeks after the first dose. Peripheral B-cell depletion was sustained for at least 6 months, and in approximately 4% of RA patients, peripheral B-cell depletion was sustained for more than 3 years after a single course of rituximab treatment. Total IgG, IgA, and, more specifically, IgM levels were lower 24 weeks after the first cycle of rituximab treatment (2.8%, 0.8% and 10% below the lower limit of normal, respectively). However, the clinical consequences of this decrease in immunoglobulin levels in RA patients are not clear at this time. Treatment with rituximab in patients with RA was also associated with a decreased level of inflammation markers. In patients with granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA) treated with rituximab, CD19 B-cells in peripheral blood were depleted to less than 10 cells/μl after the first two infusions. By month 6, approximately 84% of patients had the same level of peripheral blood CD19 B-cells, and by month 12, 81% of patients demonstrated signs of B-cell return with counts > 10 cells/μL. By Month 18, the majority of patients (87%) had counts > 10 cells/μL.
• Targets: B-lymphocyte antigen CD20