Reditux

Abstract: There is paucity of data on infusion related hypersensitivity reactions (IRHR) pattern of bio-similar rituximab in B-cell lymphoma patients. As bio-similar molecules are independently developed monoclonal antibodies, they are likely to differ in immunogenicity and therefore, the hypersensitivity data of the innovator rituximab may not be directly applicable to patients treated with the biosimilar rituximab molecule. We analysed our data of 256 patients of B cell lymphoid neoplasm who received bio-similar rituximab (Reditux) based chemo-immunotherapy for their treatment. Total 56/256 (21.8%) patients had ≥ grade II IRHR with first dose of rituximab. Grade II reactions were seen in 32/256 (12.5%) cases, grade III and grade IV reactions were seen in 21/256 (8.2%) and 3/256 (1.2%) cases, respectively. Rituximab was withdrawn from all further therapy in only 2 patients due to grade IV IRHR after attempting re-challenge of the drug under intensive monitoring. There was no difference in complete response rates in patients with or without IRHR during their first rituximab infusion. The IRHRs with bio-similar rituximab noted in our study were comparable with the previously published reactions associated with the original rituximab.

Abstract: Rituximab (anti-CD20 monoclonal antibody) has shown to improve symptoms in rheumatoid arthritis (RA) patients with inadequate response to conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs). An anti-CD20 monoclonal antibody (Reditux™) developed by Dr. Reddy’s Laboratories, India, is currently approved for use both in rheumatology and oncology patients. This retrospective report evaluates the efficacy and safety data from the real-world use of Reditux™ over a 6-month period in Indian patients with RA. All consecutive moderate to severe RA patients who failed therapy with at least two DMARDs including methotrexate (MTX) for 6 months, TNFα inhibitor naive, and willing to take Reditux™ were included. They were prescribed two doses of 1 g Reditux™, at least 15 days apart, with continued stable doses of methotrexate. Efficacy and safety after 24 weeks relative to baseline was assessed using various health assessment variables. A total of 39 patients (mean age of 46 years; 67.5 % females) treated with Reditux™ were evaluated. Statistically significant differences were observed in mean changes of DAS28-CRP, DAS28-ESR, SDAI, HAQ and Patient Global Assessment scores from baseline to 24 weeks (p < 0.0001 for all). Average steroid use per week also significantly reduced at 24 weeks (p = 0.0002). There was no significant gender difference. Mean changes in SDAI, HAQ and Patient Global Assessment scores for patients on steroids were significantly different from those not on steroids (p < 0.05 for all). At 24 weeks, 97 % of patients achieved ACR20 response demonstrating the efficacy of Reditux™ treatment. The treatment was well tolerated by patients without any clinically relevant serious adverse events over 24 weeks. Though limited by number of patients and retrospective in nature, this analysis serves as a real-world evidence of efficacy and safety of Dr. Reddy’s rituximab (Reditux™) in the treatment of csDMARD-failed patients with RA over a 6-month period.

Abstract: using the results of the studies. In DLBCL patients, VSS and T1⁄2 − β of RedituxTM are about 80 % lower than what was reported for MabTheraTM. With reason, Gota et al. suggest that RedituxTM pharmacokinetics may be altered by tumor burden, even if no influence of tumor was observed in their study. The influence of tumor burden is usually explained by target-mediated drug disposition (TMDD), a mechanism by which part of antibody elimination is mediated by target antigen burden [2]. For rituximab, increased volumes of distribution in DLBCL patients are associated with decreased concentrations and increased T1⁄2 − β. This phenomenon may be due to retention of rituximab by its tumor target antigen, a phenomenon which was previously suspected for trastuzumab [3] and bevacizumab [4]. Therefore, differences between RedituxTM and MabTheraTM pharmacokinetics might be explained by differences in interaction with their target antigen. An alternate hypothesis explaining differences in pharmacokinetic parameters between studies is the existence of various techniques used to measure the rituximab concentration. Differences in methods may lead to differences in pharmacokinetic parameters [5]. An overestimation of rituximab concentrations would have led to an underestimation of the volumes of distribution. In addition, differences in fractions detected by various assays can lead to differences in T1⁄2 − β estimation. Assays measuring both unbound (“free”) and bound to the target antigen fractions can lead to higher T1⁄2 − β estimation than assays measuring only unbound fraction [5]. A comparison of the analytical technique used by Gota et al. with those previously used to study rituximab pharmacokinetics is therefore needed before the results of this study can be compared with those reported for the originator. Dear editor,