CD38 antibody (Azide Free)
- Known as:
- CD38 (anti-) (Azide Free)
- Catalog number:
- 10r-cd38cmsp
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- CD38 antibody (Azide Free)
Related genes to: CD38 antibody (Azide Free)
- 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: CD38 antibody (Azide Free)
Related articles to: CD38 antibody (Azide Free)
- Multiple myeloma (MM) is a plasma cell malignancy, and extramedullary plasmacytoma (EMP) is associated with an aggressive biology and poor outcomes. B-cell maturation antigen (BCMA)-directed chimeric antigen receptor T-cell (CAR-T) therapy has shown substantial activity in relapsed/refractory MM (RRMM); however, evidence in patients with EMP, particularly after prior BCMA CAR-T exposure, remains limited. The present study describes the case of a 38-year-old man with RRMM and extensive cranial EMP who progressed after multiple prior therapies, including proteasome inhibitor- and immunomodulatory drug-based regimens, anti-CD38 therapy, carfilzomib-based therapy and a previous non-humanized BCMA CAR-T product. Due to rapidly progressive disease, the patient received bridging cytoreduction followed by fully humanized BCMA CAR-T therapy (equecabtagene autoleucel). After infusion, serum and urine M-protein levels rapidly declined and the craniofacial mass regressed clinically and radiographically. The patient achieved stringent complete response with durable control of extramedullary disease during follow-up. The present case suggests that fully humanized BCMA CAR-T therapy may remain effective in selected patients with RRMM and EMP, even after prior non-humanized BCMA CAR-T failure. These findings support further investigation into retreatment strategies and post-CAR-T maintenance approaches. - Source: PubMed
Publication date: 2026/09/08
Zhang RunfengCheng LiliLiu JinghuaZhang LuZhuang Junling - B-cell aggregates below the meninges have been associated with progression of neurodegeneration in multiple sclerosis (MS). We aimed to investigate the frequency of different B-cell subsets and their relationship with MS severity. Also, we quantified the CXCL13 and neurofilament (NfL) plasma levels. - Source: PubMed
Lopes Lana MárciaCafasso Marcos O SHygino JoanaSacramento Priscila MSales Marisa CKasahara Taissa MLopes Larissa Cristine Sde Azevedo Carolina Alvarezda Costa Lendel CRossi Átila DSimões Bruno Francisco TeixeiraBento Cleonice A MVasconcelos Claudia Cristina - Nicotinamide adenine dinucleotide (NAD+) is a critical coenzyme in cellular metabolism, acting as a substrate for NAD+-dependent enzymes such as sirtuins, poly(ADP-ribose) polymerases (PARPs), and CD38, which are involved in essential cellular processes including DNA repair, gene expression, and mitochondrial function. Exercise has been identified as a potent modulator of NAD+ metabolism and also influencing the expression and activity of enzymes involved in NAD+ biosynthesis and consumption. Our review focuses on the molecular mechanisms through which exercise regulates NAD+ metabolic enzymes, more in relation to aerobic and resistance exercise. Evidence indicates that exercise enhances the activity of key enzymes, such as nicotinamide phosphoribosyltransferase (NAMPT) and sirtuins, thereby improving mitochondrial efficiency, oxidative metabolism, and cellular homeostasis. Additionally, exercise has also been shown to mitigate the age-related decline in NAD+ levels, offering a potential strategy for addressing metabolic dysfunctions and age-associated diseases. Despite these findings, the exact molecular pathways underlying the exercise-induced modulation of NAD+ metabolism remain unclear and require further investigation. - Source: PubMed
Publication date: 2026/09/07
Anas Sundus HabibaKhan Sohrab AhmedAhmed Syed SuhaibMuruganantham PunithaMadar Inamul Hasan - Acute Myeloid Leukemia (AML) is a prevalent and aggressive hematologic cancer driven by leukemic stem cells and immune evasion. Among its subtypes, Mixed Lineage Leukemia-AF9 (MLL-AF9)- rearranged AML is exceptionally lethal, with B-cell lymphoma 2 (Bcl2), a key anti-apoptotic protein, supporting leukemic survival and immune dysfunction. Targeting Bcl2 in this context is crucial for dismantling oncogenic circuits and restoring immune activity. Here, we have synthesized, de novo, IL-3 receptor alpha chain (IL-3Rα, commonly known as cluster of differentiation 123 or CD123) targeted aptamer-tethered liposomal nanocarriers (CD123-si-Bcl2@LNPs) encapsulating Bcl2 siRNA (CD123-si-Bcl2@LNPs) for selective AML targeting, survival disruption, and immune restoration. Mechanistic studies established a previously uncharacterized signaling axis wherein the MLL-AF9 fusion oncoprotein induces the overexpression of the transcription factor c-Myb. This induced c-Myb binds directly to the Bcl2 promoter, upregulating Bcl2 expression and enhancing both STAT3 expression and its Ser727 autophosphorylation. Consequently, this pathway amplifies IL-6-driven immunosuppression and dampens NK and CD8⁺ T cell responses. Nanocomposite-mediated disruption of this specific axis successfully reversed these oncogenic and immunosuppressive signals. Therapeutic efficacy was evaluated using a patient-derived xenograft (PDX) model, generated by retroviral MLL-AF9 overexpression in CD34⁺/CD38⁻ sorted leukemic stem cells from AML patients and engraftment into NOD/SCID mice. CD123-si-Bcl2@LNPs significantly reduced leukemic burden in vivo. Bcl2 siRNA encapsulated liposomal nanoparticles demonstrated robust Bcl2 knockdown, apoptosis induction, and impaired leukemic self-renewal across in vitro and in vivo models. Post-treatment immune profiling revealed enhanced NK cell (CD56⁺) expression and reversal of T cell exhaustion, with CD8⁺ T cell activation marked by downregulation of CTLA-4. Differentiation marker analysis revealed decreased CD45+ and c-KIT+ expression, accompanied by an upregulation of the myeloid monocyte differentiation marker CD11b, indicating myeloid maturation and a reduction in leukemic stemness. This dual-action therapeutic strategy simultaneously targets survival and immune evasion pathways in MLL-AF9-positive AML cells by the treatment of CD123-si-Bcl2@LNPs, offering a promising, precision-guided nano-immunotherapeutic strategy for future translational potential for MLL-AF9-positive acute myeloid leukemia. STATEMENT OF SIGNIFICANCE: •The CD123 aptamer-targeted liposomal nanocarrier facilitates precise siRNA delivery in acute myeloid leukemia (AML), significantly enhancing the transfection efficiency and stability of Bcl2 siRNA. •siRNA nanotherapy reveals a novel immune-evasion axis involving c-Myb, Bcl2, and STAT3 axis which is critical for the progression of AML. •Targeted silencing of Bcl2 disrupts the survival networks of leukemic stem cells. •Nano-immunotherapy revitalizes the antitumor activity of natural killer (NK) cells and CD8⁺ T-cells. •Liposomal siRNA therapy effectively suppresses MLL-AF9 leukemia in NOD/SCID patient-derived xenograft (PDX) mouse models. - Source: PubMed
Publication date: 2026/09/20
Ayoub MohdGhosh DevangiSahu Vikas KumarBiswal LikuMalhotra PankajKarmakar SurajitChoudhury Subhasree Roy - Histone lactylation is an epigenetic modification that connects lactate metabolism with protein function. Our study identified lactate enhances the protein lactylation level not only in Myeloid-derived suppressor cells (MDSCs) of tumor-bearing mice, but also in the tumor tissues of lung cancer patients. This modification led to upregulation of CD38 expression and enhanced the immunosuppressive function of MDSCs. Mechanistically, CD38 promoted immunosuppression by depleting NAD⁺, and treatment with CD38 inhibitor or siRNA-mediated knockdown of CD38 in MDSCs delayed tumor progression. H3K18la is enriched at CD38 promoter region, with p300, HDAC1-3, and BRD4 identified as key epigenetic regulators in this process. Our findings reveal the critical role of the lactate-CD38-NAD⁺ axis in regulating MDSC immunosuppressive function and establish histone lactylation as an epigenetic mechanism controlling CD38 expression. - Source: PubMed
Publication date: 2026/09/18
Dai YaoDai HaiyanWang YahuiDa WenxinZhang YanZhu WeiWang DeqiangWang ShengjunMa Jie