MECHANISM OF ACTION
Targeted and precisely delivered B-cell therapy
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This animated video brings the immune system to life with a molecule's eye view of KESIMPTA
KESIMPTA® (ofatumumab) mechanism of action
KESIMPTA is thought to work by selectively binding to sites on both the small and large extracellular loops of CD20.1
KESIMPTA causes CD20+ B cells to be vulnerable to both immediate and delayed B-cell lysis by mechanisms such as complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity1
When delivered subcutaneously, KESIMPTA is thought to promote preferential depletion of B cells in the lymph nodes.2,3
Preclinical evidence suggests KESIMPTA may spare B cells in the spleen that help maintain immune function.4,5
The precise mechanism by which KESIMPTA exerts its therapeutic effects is unknown.
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Targeted and Precisely Delivered Therapy: Understanding KESIMPTA Mechanism of Action
Watch a video with an expert perspective on
the KESIMPTA mechanism of action
Targeted and Precisely Delivered Therapy:
Understanding KESIMPTA Mechanism of Action
Subcutaneous, targeted, and precisely delivered therapy that provides rapid B-cell depletion6,7
B-cell depletion sustained over the dosing period
B-cell depletion sustained over
the dosing period
Reduction in B cells was seen as early as 1 week after treatment initiation2
The CD19+ B-cell counts remained below LLN for approximately 97% of patients in ASCLEPIOS I and 92% of patients in ASCLEPIOS II from 12 weeks through 120 weeks while on KESIMPTA treatment2
B-cell repletion upon
Data from RMS clinical studies indicate B-cell recoveries over the LLN in at least 50% of patients in 24 to 36 weeks post-treatment discontinuation
Modeling and simulation for B-cell repletion corroborates these data, predicting median time to B-cell recovery of 40 weeks post-treatment discontinuation
*Actual KESIMPTA patient who was compensated for their time. Individual results may vary.
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IgG=immunoglobin G; LLN=lower limit of normal; MOA=mechanism of action; RMS=relapsing multiple sclerosis; SC=subcutaneous.
References: 1. Gupta IV, Jewell RC. Ofatumumab, the first human anti-CD20 monoclonal antibody for the treatment of B cell hematologic malignancies. Ann NY Acad Sci. 2012;1263(1):43-56. 2. Kesimpta [package insert]. East Hanover, NJ: Novartis Pharmaceuticals Corp; 2020. 3. Huck C, Leppert D, Wegert V, et al. Low-dose subcutaneous anti-CD20 treatment depletes disease relevant B cell subsets and attenuates neuroinflammation. J Neuroimmune Pharmacol. 2019;14(4):709-719. 4. Torres JB, Roodselaar J, Sealey M, et al. Distribution and efficacy of ofatumumab and ocrelizumab in humanized-CD20 mice following subcutaneous or intravenous administration. P2.2.052. Poster presented at: American Academy of Neurology Annual Meeting; May 4-10, 2019; Philadelphia, PA. 5. Theil D, Smith P, Huck C, et al. Imaging mass cytometry and single-cell genomics reveal differential depletion and repletion of B-cell populations following ofatumumab treatment in cynomolgus monkeys. Front lmmunol. 2019;10:1-11. 6. Hauser SL, Bar-Or A, Cohen JA, et al. B-cell depletion and efficacy outcomes with ofatumumab: subgroup analysis from the pooled phase 3 ASCLEPIOS I and II trials. P7.1-013. Poster presented at: American Academy of Neurology Annual Meeting; May 4-10, 2019; Philadelphia, PA. 7. Hauser SL, Bar-Or A, Cohen JA, et al; for the ASCLEPIOS I and ASCLEPIOS II trial groups. Ofatumumab versus teriflunomide in multiple sclerosis [supplemental appendix]. N Engl J Med 2020;383(6):546-557.