Anti-Human CD38 FITC 100 tests
- Known as:
- Antibody toHuman CD38 fluorecein 100 tests
- Catalog number:
- 11-0389-42
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD38 FITC 100 tests
Related genes to: Anti-Human CD38 FITC 100 tests
- Gene:
- CD38 NIH gene
- Name:
- CD38 molecule
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4p15.32
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2014-11-18
Related products to: Anti-Human CD38 FITC 100 tests
Related articles to: Anti-Human CD38 FITC 100 tests
- The therapeutic goal in multiple myeloma (MM) is changing from long-term disease control to a potential cure. While anti-CD38-containing quadruplets have improved outcomes, relapses continue to occur in many patients. In recent years, advancements in immunotherapy have fundamentally changed this paradigm. Bispecific antibodies (BsAbs) and chimeric antigen receptor T-cells (CAR T-cells) have deepened responses and achieved sustained MRD negativity in an unprecedented way, raising the possibility of curing MM in a subset of patients. Recently, the International Myeloma Society (IMS) reached a consensus and discussed a framework to define cure. This review examines how novel immunotherapies are redefining frontline strategies in newly diagnosed MM (NDMM) and attempts to summarize how BsAbs, CAR T-cells, and cereblon E3 ligase modulators (CELMoDs) can be integrated into induction, consolidation, and maintenance phases. It also discusses the evolving role of autologous stem cell transplant (ASCT) in the immunotherapy era and MRD-guided treatment and discontinuation strategies. Together, this review attempts to provide a roadmap to fulfill the criteria for cure. - Source: PubMed
Publication date: 2026/09/25
Joshi AdvaitPuliafito Benjamin RCirstea Diana DBranagan Andrew RGustine Joshua NShome RajibPanaroni CristinaYee Andrew JRaje Noopur S - Multiple myeloma is a plasma cell malignancy associated with heterogeneous clinical outcomes. The majority of patients are diagnosed during their seventh decade and often present with age-related comorbidities and organ dysfunction. Myeloma therapeutic landscape is rapidly evolving with the introduction of immune-based therapies, including monoclonal and bispecific antibodies and chimeric antigen receptor (CAR) T-cell therapies targeting CD38, BCMA, and GPRC5D. These novel therapies have led to deeper and more durable responses and have raised the possibility of functional or definitive cure. However, older and frail patients continue to experience poorer outcomes, higher toxicity rates, and substantial treatment attrition, representing a major unmet clinical challenge. In this review, we discuss current approaches to the assessment and management of frailty in patients with multiple myeloma, with a focus on optimizing frontline therapy and treatment at relapse in the era of the possible achievement of a cure. We highlight emerging data on cellular therapies in this population and the importance of individualized, goal-directed treatment strategies aimed at balancing efficacy, tolerability, and quality of life. - Source: PubMed
Publication date: 2026/09/25
George ThomasSzalat Raphael E - Monoclonal antibodies (mAbs) and antibody-drug conjugates (ADCs) have significantly expanded the therapeutic landscape of multiple myeloma (MM), contributing to deeper and more durable responses and meaningful survival benefits across the continuum of the disease. CD38-targeting mAbs are now integral to frontline regimens, while ADCs introduce a complementary strategy by enabling targeted delivery of cytotoxic payloads, most notably through B-cell maturation antigen (BCMA). However, the clinical integration of these agents has revealed new resistant mechanisms, including antigen loss, immune exhaustion, and the emergence of cross-resistance across BCMA-directed therapies. Furthermore, challenges in the sequencing of treatments have emerged, as novel immunotherapies have also become available in the early relapse setting. This contemporary review examines the evolving role of mAbs and ADCs in MM, addressing both current status and directions for future research in the field. - Source: PubMed
Publication date: 2026/09/25
Ntanasis-Stathopoulos IoannisTerpos EvangelosDimopoulos Meletios-Athanasios - Multiple myeloma cells are uniquely dependent on proteostasis due to their exceptionally high immunoglobulin synthesis and protein turnover, rendering them hypersensitive to disruptions in protein degradation. Proteasome inhibitors targeting the 20 S catalytic core exploit this vulnerability and remain a therapeutic cornerstone in newly diagnosed and relapsed/refractory settings, anchoring both triplet and quadruplet regimens that incorporate anti-CD38 monoclonal antibodies, immunomodulatory agents, antibody-drug conjugates, and nuclear export inhibitors. Beyond the 20 S core, emerging targets, including the 19 S regulatory particle, deubiquitinating enzymes, and the E1-E2-E3 ubiquitination cascade, offer opportunities to intensify proteotoxic stress and overcome resistance. Targeted protein degradation platforms, including CELMoDs, proteolysis targeting chimeras, molecular glues, and proteasome cap-recruiting chimeras, further expand the therapeutic repertoire. Compensatory stress responses involving autophagy, the unfolded protein response, and the bone marrow microenvironment modulate therapeutic vulnerability. Collectively, these advances position proteostasis not as a single druggable target but as an integrated therapeutic network amenable to rational, biomarker-informed combination strategies in multiple myeloma. - Source: PubMed
Publication date: 2026/09/25
Song YanTheprungsirikul PoyGulla AnnamariaAnderson Kenneth C - Smoldering multiple myeloma (SMM) is an asymptomatic precursor of multiple myeloma characterized by marked heterogeneity in the risk of progression. Current management relies on clinical risk stratification to identify patients who might benefit from early intervention. Models such as the 20/2/20 score and its International Myeloma Working Group refinement incorporate tumor burden and cytogenetic abnormalities, whereas emerging approaches integrating dynamic biomarkers, circulating tumor cells, genomic alterations, and immune signatures could further improve the prediction of progression if validated in larger cohorts. Randomized trials suggest that early treatment with lenalidomide-based regimens or anti-CD38 monoclonal antibodies delays progression and possibly improves survival in high-risk SMM, and daratumumab has been approved as an early intervention in high-risk SMM. More intensive immunotherapy-based strategies can achieve high rates of sustained measurable residual disease negativity, which might translate into durable disease control or even a cure. Future management will likely depend on biologically informed, risk-adapted strategies to balance early treatment benefits against overtreatment, together with safety profile and patients' preferences. - Source: PubMed
Publication date: 2026/09/25
Puertas BorjaAlejo ElenaMateos María-Victoria