Anti_Human, mab CD38 Source Mouse
- Known as:
- Anti_Human, mab CD38 Source Mouse
- Catalog number:
- 101-M306
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Human mab CD38 Source Mouse
Related genes to: Anti_Human, mab CD38 Source Mouse
- 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, mab CD38 Source Mouse
Related articles to: Anti_Human, mab CD38 Source Mouse
- While outcomes for children and adolescents with T-cell acute lymphoblastic leukemia (T-ALL) have improved significantly with contemporary therapy, outcomes for newly diagnosed adults and all patients with relapsed or refractory (r/r) disease remain poor. Improved understanding of T-ALL genomics and the integration of novel agents into treatment have the potential to improve outcomes further by enhancing risk stratification and improving salvage rates for those with r/r disease. In this review, we will discuss landmark genomic studies that have identified therapeutic targets in T-ALL, shed further light on the early-T precursor phenotype, and described novel genomic subtypes of T-ALL. We will further discuss recent clinical trials investigating the role of nelarabine and bortezomib into front-line therapy for T-ALL, highlighting the benefit of nelarabine for pediatric and adolescent/young adult patients with T-ALL seen on the Children's Oncology Group trial AALL0434 (4-year disease-free survival 92.2% for the Capizzi methotrexate + nelarabine arm). Finally, we will address new classes of targeted small molecule inhibitors, immunotherapeutics, and chimeric antigen receptor T-cell therapies under investigation in r/r T-ALL. We focus on recent trials incorporating novel immunotherapies, including a phase 2 trial of the anti-CD38 monoclonal antibody daratumumab in combination with chemotherapy which demonstrated an overall response rate of ∼80% as well as numerous early-phase chimeric antigen receptor T-cell trials with response rates exceeding 90%. - Source: PubMed
Publication date: 2026/04/28
Summers Ryan JNewman HaleyTeachey David T - Relapsed/refractory multiple myeloma (RRMM) remains a clinical challenge despite therapeutic advances. CD38-directed chimeric antigen receptor T-cell (CAR-T) therapy, especially dual-target CD38/BCMA constructs, represents an emerging immunotherapeutic strategy. This systematic review and meta-analysis aimed to evaluate the efficacy and safety of CD38-directed CAR-T in RRMM. - Source: PubMed
Publication date: 2026/04/29
Xu XinlongDong ChangGuo JiashuoChang XiaolinZhang YuGou ShutingXue LiyingLi Jie - - Source: PubMed
Publication date: 2026/05/01
Laganà AlessandroBreccia MatteoElia LoredanaScalzulli EmiliaBisegna Maria LauraIelo ClaudiaBuffolino SoniaDi Lascio AttilioGermano Concetta AnnaIntoppa StefaniaMilani Maria LauraMartelli MaurizioBreccia MassimoDe Propris Maria Stefania - Multiple myeloma (MM) develops within a profoundly immunosuppressive bone marrow (BM) microenvironment. CD38, a multifunctional ectoenzyme highly expressed on malignant plasma cells, contributes to this niche by degrading nicotinamide adenine dinucleotide (NAD) into ADPR, which fuels adenosine (ADO) production through CD38/CD203a/CD73 enzymatic pathway. CD38_targeting monoclonal antibodies (mAbs), including daratumumab (DARA) and isatuximab (ISA), exert antitumor activity through direct cytotoxicity and immune modulation; however, resistance to these agents remains a major clinical challenge. Understanding how CD38 enzymatic activity and adenosinergic metabolism evolve during therapy is essential for improving treatment efficacy. - Source: PubMed
Publication date: 2026/04/29
Horenstein Alberto LFrerichs Kristine AFaini Angelo Cvan de Donk Niels W C JMalavasi Fabio - Persistent renal dysfunction after haematologic remission in monoclonal immunoglobulin deposition disease creates uncertainty regarding treatment intensity when clinical parameters do not distinguish reversible injury from established structural remodelling. We report a 34-year-old man with light- and heavy-chain deposition disease who presented with serum creatinine 1.8 mg/dL and heavy proteinuria (urine protein-to-creatinine ratio 5.0 g/gCr). After cyclophosphamide, bortezomib and dexamethasone therapy, haematologic parameters improved and proteinuria decreased; however, renal function continued to worsen, and serum creatinine increased to 4.1 mg/dL before autologous stem cell transplantation. Despite a deep haematologic response after transplantation, serum creatinine remained elevated at 2.7 mg/dL. A second kidney biopsy demonstrated persistent proliferative glomerular lesions with limited global sclerosis (1/56 glomeruli). Minimal residual disease remained detectable at 0.0029%, supporting additional clone-directed therapy. Following CD38-directed treatment, proteinuria resolved and minimal residual disease became undetectable, yet serum creatinine remained approximately 1.9 mg/dL with persistent microscopic haematuria. Because laboratory findings could not determine whether residual dysfunction reflected ongoing activity or fixed chronic change, a third kidney biopsy was performed. This biopsy revealed resolution of active glomerular lesions with predominance of chronic remodelling (5/32 globally sclerotic glomeruli). Therapy was discontinued, and renal function subsequently improved gradually to 1.1 mg/dL, remaining stable for more than 5 years without further therapy. Serial kidney biopsies informed two distinct therapeutic decisions-treatment escalation and subsequent discontinuation-when clinical parameters alone were insufficient to guide management. - Source: PubMed
Kakiuchi SeijiTakagi IkumiTomigaki NaruSakamoto AkimasaFujioka ShutaroHarima IsamuAkiyama HiroakiNiwa RyotaroKozuki YokoMiyata YoshiharuIwata NobukoHara ShigeoTomida Kodo