Molecular Formula | C6416H9874N1688O1987S44 |
Storage Condition | -20℃,避光 |
In vitro study | The potency of Rituximab depends primarily on its complement-dependent toxicity (CDC), complement-dependent cytotoxicity (CDCC), antibody-dependent cytotoxicity (ADCC), and apoptosis-inducing effects. Rituximab induces the death of malignant B cells in vitro. The potency of the action varies with different target cells. In vitro, the cellular changes induced by Rituximab are: p38 MAPK, NF-κB, ERK1/2, inhibition of AKT anti-apoptotic, survival signaling pathways. Rituximab is highly effective in mediating complement-dependent toxicity (CMC) of different B cell lines and malignant B cells. The CD20 binding capacity of Rituximab was concentration-dependent. |
In vivo study | Some in vivo tumor models have demonstrated that the anti-tumor activity of rituximab depends (at least in part) on complement. Rituximab can deplete B cells for several months and thus can be an effective regimen for the treatment of B cell-mediated autoimmune diseases. Rituximab is widely used in the treatment of hematological tumors and is currently in the development of drugs for the treatment of several autoimmune diseases. |