KESIMPTA®▼ (ofatumumab) is indicated for the treatment of adult patients with relapsing forms of multiple sclerosis with active disease defined by clinical or imaging features.
For full safety information, please refer to the GB KESIMPTA Summary of Product Characteristics (SmPC) and NI KESIMPTA Summary of Product Characteristics (SmPC).
KESIMPTA has demonstrated efficacy in ASCLEPIOS I and II, two identically designed clinical studies comparing a range of outcomes to active comparator teriflunomide in 1882 patients with relapsing MS.1 Read more about ASCLEPIOS study design here.
Click on the tabs below to find out the results for specific efficacy outcome measures.
Annualised relapses
KESIMPTA demonstrated a significant reduction in relapses (ASCLEPIOS primary endpoint)
Relative reduction in annualised relapses vs teriflunomide1–3
Adapted from Hauser SL, et al. 2020.1
The KESIMPTA arm achieved 0.1 relapses per year, equivalent to 1 relapse every 10 patient-years2,3
Patients on the continuous KESIMPTA arm experienced 0.05 ARR† at 4 years, equivalent to 1 relapse every 20 patient years*4
Within and between-group comparisons during the core and extension phases for ASCLEPIOS and ALITHIOS
Adapted from Kappos L, et al. 2022.4
Patients switching from teriflunomide to KESIMPTA achieved a 72% ARR reduction at 4 years4,5
Gd+ T1 and T2 lesions
KESIMPTA resulted in suppression of Gd+ T1 and T2 lesions (secondary endpoint)
Adapted from Hauser SL, et al. 20226.
Switching to KESIMPTA can help your patients gain lesion activity control6
Disability worsening
In the ALITHIOS 5-year extension, KESIMPTA showed flattening of the 6m-raw curve in the teriflunomide switch group; differences between the continuous and switch groups were not statistically significant7
Adapted from Cohen JA, et al. 2023.7
In the extension period, KESIMPTA showed high anti-inflammatory efficacy with flattening of the 6M-RAW curve in the teriflunomide switch group7
NEDA-3
No evidence of disease activity (NEDA-3) definition criteria8
NEDA-3 was determined in a post-hoc analysis of pooled ASCLEPIOS trials
Within the specified time interval, patients who achieved NEDA-3 experienced none of the following:
6-month CDW
Confirmed relapse
Gd+ T1 lesions AND new or enlarging T2 lesions
In ALITHIOS, nearly 80% of patients in the continuous KESIMPTA group had NEDA-3‡4
Adapted from Kappos L, et al. 2022.4
Effect of KESIMPTA on individual NEDA-3 components4
Cumulatively, over 4 years, more patients continuously using KESIMPTA were free of Gd+ T1 lesions, new or enlarging T2 lesions, confirmed relapses and 6-month CDW than patients switching from teriflunomide.4
Adapted from Kappos L, et al. 2022.4
With earlier initiation of KESIMPTA, more patients showed no evidence of disease activity vs patients switching from teriflunomide over 4 years4
Other secondary endpoints
Patients receiving continuous KESIMPTA for up to 5 years demonstrated significantly lower levels of % brain volume change (BVC) than those who switched from teriflunomide (<1.5% vs ≥1.5% loss)7
% BVC over 5 years
Adapted from Cohen JA, et al. 2023.7
Statistically significant between-group comparison at each year for % BVC. % BVC estimates are obtained from a mixed model for repeated measures.
At 5 years, earlier KESIMPTA initiation resulted in significantly lower levels of % brain volume change vs later switch from teriflunomide to KESIMPTA7
KESIMPTA demonstrated a favourable trend but non-significant difference in 6-month CDI vs teriflunomide1,9
6-month confirmed disability-improvement (CDI)§1,9
Adapted from Hauser SL, et al. 2019.9
The difference in 6-month CDI between the two treatment groups did not reach statistical significance.
Based on a prespecified pooled analysis of the results of the ASCLEPIOS I and II Phase III pivotal trials for KESIMPTA.
KESIMPTA demonstrated significant and consistent reduction in serum NfL levels with a reduction of up to 24% at Month 24 vs teriflunomide‖1,9
Neurofilament light chain (NfL) concentration in serum‖1,9
Adapted from Hauser SL, et al. 2019.9
Learn more about how KESIMPTA’s proven efficacy is supported by a generally well-tolerated safety profile
*Obtained from fitting a piecewise negative binomial model for the time period core phase and extension phase with log-link, adjusted for treatment and region as factors, number of relapses in previous year, baseline EDSS, baseline number of Gd-enhancing lesions and the patient’s age at baseline as covariates. The natural log of the time-in-study (in years) by period is used as offset to annualise the relapse rate in each period.1
†Estimated from fitting a piecewise negative binomial model for the time period core phase and extension phase with log-link, adjusted for treatment and region as factors, baseline number of T1 Gd-enhancing lesions and patient’s age at baseline as covariates. The natural log of the number of scans with evaluable Gd-enhancing lesion counts by period is used as offset to obtain the lesion rate per scan in each period. Baseline variables are from the core study baseline.6
‡Re-baseline at the entry of extension was performed. All p-values are nominal p-values. N=The total number of patients in the treatment group excluding those who discontinued treatment early for reasons other than lack of efficacy or death and had NEDA before early discontinuation; NEDA-3 is defined as no 6-month CDW, no confirmed MS relapse, no new or enlarging T2 lesions compared to baseline and no T1 Gd-enhancing lesions. Statistical model used logistic regression adjusting for treatment and region as factors and age, baseline EDSS, number of Gd-lesions at baseline as covariates.4
§Analysed via a Cox regression model. 6-month confirmed disability improvement was defined as a decrease from baseline in EDSS score sustained for at least 6 months.1
¶Statistical test uses significance (2-sided) level at 0.04875.
‖ASCLEPIOS I: 7% (8.8 [95% CI 8.5–9.1] vs 9.4 [95% CI 9.1–9.8]) 27% (7.0 [95% CI 6.7–7.3] vs 9.6 [95% CI 9.2–10.1] 23% (6.9 [95% CI 6.6–7.2] vs 9.0 [95% CI 8.6–9.5]), ASCLEPIOS II: 11% (8.9 [95% CI 8.6–9.2] vs 10.0 [95% CI 9.7–10.4]) 26% (7.1 [95% CI 6.8–7.4] vs 9.5 [95% CI 9.1–10.0]) 24% (6.8 [95% CI 6.5–7.1]) vs 9.0 [95% CI 8.6–9.4]).1
6m-CDW, 6-month CDW; 6m-PIRA, 6-month confirmed PIRA; 6m-RAW, 6-month confirmed RAW; 6m-sPIRA, 6-month confirmed sustained PIRA; ARR, annualised relapse rate; BVC, brain volume change; CDI, confirmed disability improvement; CDW, confirmed disability-worsening; CI, confidence interval; EDSS, expanded disability status scale; Gd, gadolinium; Gd+, gadolinium enhancing; HR, hazard ratio; K-M, Kaplan–Meier; MS, multiple sclerosis; NEDA-3, no evidence of disease activity-3; NfL, neurofilament light chain; OR, odds ratio.
References
- Hauser SL, et al. New Engl J Med 2020;383(6):546–557, and supplementary material.
- KESIMPTA (ofatumumab) Summary of Product Characteristics, Great Britain; July 2022.
- KESIMPTA (ofatumumab) Summary of Product Characteristics, Northern Ireland; July 2022.
- Kappos L, et al. Poster EPR161 presented at the European Academy of Neurology. June 2022.
- Data on file. T056 Table 3-1.2_ARR. Novartis Pharmaceuticals Corp; East Hanover, NJ.
- Hauser SL, et al. Poster P5.004 presented at the American Academy of Neurology (ANN). April 2022.
- Cohen JA, et al. Poster P009 presented at the American Academy of Neurology (AAN). April 2023.
- Data on file. OMB157. Novartis Pharmaceuticals Corp, Statistical Overview, East Hanover, NJ. December 2019.
- Hauser SL, et al. Oral presentation 336 presented at the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS), September 2019; Stockholm, Sweden.
