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Does IVIG Protect BCMA-directed antibody Myeloma?
Does IVIG protect BCMA-directed bispecific antibody in myeloma? What is IVIG therapy? Wby is IVIG therapy needed in the first place?
Why are BCMA-directed antibodies MM therapies?
BCMA-directed bispecific antibodies are being used as a treatment option for multiple myeloma, particularly in patients who have relapsed or are refractory to other therapies.
What are BCMA-directed bispecific antibodies?
“Teclistamab and elranatamab are examples of BCMA-directed bispecific antibodies that have been approved for the treatment of relapsed or refractory multiple myeloma.”
What is intravenous immunoglobulin (IVIG),when will it be prescribed, and how does it work?
As the top study linked and excerpted below explains, BCMA-directed therapies are effective “off the shelf” therapy for RR/MM patients.
Unfortunately, they can result is serious infections. Conventional MM oncology’s solution is to try to enhance the immune system for MM patients undergoing BCMA-directed therapies with intravenous IVIG.
The second study linked below found that “In recipients of BCMA-directed bsAb, IVIG supplementation was associated with an improved clinical outcome, including favorable IFS and OS…”
Are you considering BCMA-directed bispecific antibody therapy? If you would like to learn more about evidence-based but non-conventional immune health therapies email me at David.PeopleBeatingCancer@gmail.com.
Good luck,
David Emerson
- MM Survivor
- MM Cancer Coach
- Director PeopleBeatingCancer
Comparison of infectious complications with BCMA-directed therapies in multiple myeloma
B-cell-maturation-antigen (BCMA)-directed therapies are highly active for multiple myeloma, but infections are emerging as a major challenge.
In this retrospective, single-center analysis we evaluated infectious complications after
- BCMA-targeted chimeric-antigen-receptor T-cell therapy (CAR-T),
- bispecific-antibodies (BsAb) and
- antibody-drug-conjugates (ADC).
The primary endpoint was severe (grade ≥3) infection incidence. Amongst 256 patients,
- 92 received CAR-T,
- 55 BsAb and
- 109 ADC.
The incidence of severe infections was higher with BsAb (40%) than CAR-T (26%) or ADC (8%), including grade 5 infections (7% vs 0% vs 0%, respectively).
Comparing T-cell redirecting therapies, the incidence rate of severe infections was significantly lower with CAR-T compared to BsAb at 1-year (incidence-rate-ratio [IRR] = 0.43, 95%CI 0.25−0.76, P = 0.004).
During periods of treatment-emergent hypogammaglobulinemia, BsAb recipients had higher infection rates (IRR:2.27, 1.31−3.98, P = 0.004) and time to severe infection (HR 2.04, 1.05–3.96, P = 0.036) than their CAR-T counterparts.
During periods of non-neutropenia, CAR-T recipients had a lower risk (HR 0.44, 95%CI 0.21−0.93, P = 0.032) and incidence rate (IRR:0.32, 95% 0.17–0.59, P < 0.001) of severe infections than BsAb.
In conclusion, we observed an overall higher and more persistent risk of severe infections with BsAb. Our results also suggest a higher infection risk during periods of hypogammaglobulinemia with BsAb, and with neutropenia in CAR-T recipients…”
Effect of Intravenous Immunoglobulin (IVIG) Supplementation on infection-free survival in recipients of BCMA-directed bispecific antibody therapy for multiple myeloma
Abstract
The main objective of this multi-institutional study is to understand the effect of primary intravenous immunoglobulin (IVIG) replacement on clinical outcomes in recipients of BCMA-directed bispecific antibody (bsAb), where infection remains an important cause of morbidity and mortality.
This is a retrospective study of patients treated with either standard of care teclistamab or BCMA-directed investigational bsAb between Nov 2017 and Dec 2023. Primary IVIG prophylaxis was defined as starting IVIG prior to first documented infection.
All analyses were adjusted for immortal-time bias inherent in this grouping. A total of 225 patients were included in this analysis. Primary IVIG prophylaxis was defined as starting IVIG prior to first documented infection.
The median follow-up of patients treated with and without primary IVIG prophylaxis was, 9 and 11 months, respectively.
The cumulative incidence of all grade infections at 12 months with and without primary IVIG prophylaxis were 56% (95%CI 40%,78%) and 60% (95% CI 48%, 76%); p = 0.72, respectively.
The 12-month cumulative incidence of ≥ grade 3 infections was 35% (95% CI 21%, 57%) with primary IVIG prophylaxis and 45% (95% CI 34%, 60%) without; p = 0.37. The median infection free survival (IFS) for all-grade infections was 7.7 (95% CI 3.3, 14) months with primary
IVIG prophylaxis and 3 (95% CI 2.6, 4.5) months without (p = 0.021). The median ≥ grade 3 IFS was 14 (95% CI 8.8, NR) and 7.5 (95% CI 6.1, 14) months, with and without primary IVIG respectively; p = 0.022.
Patients on primary IVIG prophylaxis had a superior progression-free-survival (PFS) [median PFS 15 vs 8 months; p = 0.026] and overall-survival (OS) [median OS 16 vs 44 months; p = 0.007].
On multivariate analysis, primary IVIG prophylaxis was independently associated with improved OS (HR = 0.37; p = 0.021), while the presence of extra-medullary (HR = 2.71; p = <0.001) and high-risk disease (HR = 1.88; p = 0.031) conferred poor outcomes.
In recipients of BCMA-directed bsAb, IVIG supplementation was associated with an improved clinical outcome, including favorable IFS and OS…
In conclusion, while we await clinical trials that demonstrates concrete benefits of IVIG prophylaxis in the era of the novel treatment strategies such as CAR T and bsAb therapies, our study demonstrates that effective supportive care measures such as these may further enhance therapeutic efficacies of these agents.”
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