Although the anti- @entity2225 antibody Rituximab has revolutionized the treatment of @entity1893 ( @entity1893 ), resistance to treatment still existed. Thus, strategies for suppressing Rituximab-resistant NHLs are urgently needed. Here, an anti- @entity2225 nanocluster (ACNC) is successfully constructed from its type I and type II mAb (Rituximab and 11B8). These distinct anti- @entity2225 mAbs are mass grafted to a short chain polymer ( @entity12279 ). Compared with parental Rituximab and 11B8, the ACNC had a reduced "off-rate". Importantly, ACNC efficiently inhibited Rituximab-resistant @entity706 in both disseminated and localized @entity1 @entity1893 xenograft models. Further results revealed that ACNC is significantly potent in inducing caspase-dependent apoptosis and lysosome-mediated @entity204 ( @entity204 ). This may help explain why ACNC is effective in suppressing @entity706 while Rituximab and 11B8 are not. Additionally, ACNC experienced low clearance from peripheral blood and high intratumor accumulation. This improved pharmacokinetics is attributed to the antibody-antigen reaction (active targeting) and enhanced permeability and retention (ERP) effect (passive targeting). This study suggested that ACNC might be a promising therapeutic agent for treatment of @entity706 .

Suppression of Rituximab-resistant B-cell lymphoma with a novel multi-component anti- XXXX mAb nanocluster.

@entity1 :: ('9606', 'Species') :: ['human'] @entity706 :: ('MESH:D008223', 'Disease') :: ['rituximab-resistant lymphomas', 'rituximab-resistant lymphoma', 'lymphomas'] @entity12279 :: ('MESH:D011094', 'Chemical') :: ['polyethylenimine'] @entity2225 :: ('54474', 'Gene') :: ['CD20'] @entity1893 :: ('MESH:D008228', 'Disease') :: ['NHL', 'Non-Hodgkin Lymphoma'] @entity204 :: ('MESH:D003643', 'Disease') :: ['PCD', 'programmed cell death']
@entity2225 :: (54474,Gene) :: ['CD20']
