MSLN Antibody
- Known as:
- MSLN Antibody
- Catalog number:
- csb-pa015044esr1hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- Gene target:
- MSLN Antibody
Related genes to: MSLN Antibody
- Gene:
- MSLN NIH gene
- Name:
- mesothelin
- Previous symbol:
- -
- Synonyms:
- CAK1, MPF
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-22
- Date modifiied:
- 2015-08-25
Related products to: MSLN Antibody
Related articles to: MSLN Antibody
- Chimeric antigen receptor (CAR) therapies have shown great success in hematological malignancies but remain largely ineffective against solid tumors such as pancreatic ductal adenocarcinoma (PDAC). A key obstacle among various aspects, is the dense stromal barrier formed by cancer-associated fibroblasts (CAFs), providing a rationale for simultaneously targeting stroma and tumor cells. Using immunohistochemistry of primary PDAC tumors and liver metastases, we confirmed high mesothelin (MSLN) expression on tumor cells, and CD70 expression on tumor cells and predominantly CAFs. Based on these results and the favorable safety profile of CAR natural killer (NK) cells over CAR T cells, we generated MSLN- and CD70-targeting IL-15-armored CAR NK cells. Both constructs mediated cytotoxicity against different pancreatic cancer and CAF cell lines with varying antigen expression , demonstrating that both, the CAR-molecule and IL-15 were required to increase functionality against more treatment-resistant cell lines. Interestingly, pooled MSLN- and CD70-CAR NK cells did not significantly improve cytolysis compared to monotherapies in an advanced 3D model or . Together these findings highlight the limitations of dual-targeting approaches and underscore the need for advanced engineering strategies to improve CAR NK cells beyond antigen targeting and cytokine support in the PDAC microenvironment. - Source: PubMed
Publication date: 2026/08/05
Gehrcken LauraOtt JasperVan den Eynde AstridLau Ho WaLiu DanaHermans ChristopheVerhezen TiasPeeters StefanieFaghel CaroleJoye PhilippeRoex GilsCampillo-Davo DianaLion EvaElvas FilipeKoljenovic SenadaDe Waele JorritHartman VeraRoeyen GeertPrenen HansLardon FilipDeben ChristopheSmits EvelienVan Audenaerde Jonas - Mesothelin (MSLN) is a cell surface glycoprotein that is often over-expressed in various malignancies of humans and has been suggested as a potential therapeutic and diagnostic target. However, its expression profile, clinical implications and drug-targeting potential are not fully understood and needs to be investigated across various cancer types. - Source: PubMed
Publication date: 2026/08/20
Sheikh Md RamjanMistry BaishakhiShafin Ridika HaqueApu AmreetaSara Tasnia HossainTasnim JarinDutta DipankarNandy AishwaryaRahman Anisur - Chimeric antigen receptor-engineered NK cells targeting mesothelin (MSLN CAR-NK) have emerged as promising off-the-shelf immunotherapeutics for multiple malignancies. However, their clinical translation remains constrained by inefficient cytotoxic potency and limited persistence. This study investigated the therapeutic potential of nicotinamide mononucleotide (NMN), a metabolic modulator known to enhance immune cell functionality, in augmenting MSLN CAR-NK cell efficacy against ovarian cancer (OC). Through systematic evaluation, we found that NMN supplementation significantly enhanced CAR-NK cell activation marker expression (CD69, NKG2D), degranulation capacity (CD107a increased by 21.7 ± 1.1%), and cytokine production (IFN-γ elevated 1.3-fold). In addition, NMN treatment potentiated MSLN CAR-NK cell-mediated cytotoxicity against MSLN target cells, achieving 32.8 ± 1.4% specific lysis at an effector-to-target ratio of 25:1, while concurrently reducing cellular apoptosis compared with controls. Mechanistic interrogation via transcriptomic profiling revealed NMN-mediated modulation of PLC-γ phosphorylation cascades and mitochondrial redox homeostasis. Notably, NMN effectively counteracted tumor microenvironment-induced mitochondrial ROS accumulation (reduced by 25.1 ± 0.8% in OC-conditioned medium). Critically, in an OVCAR8-MSLN xenograft model, adoptive transfer of NMN-preconditioned CAR-NK cells led to superior tumor control, reduced proliferation (Ki67), diminished angiogenesis (CD31), and enhanced intratumoral CAR-NK infiltration compared with controls. These findings establish NMN as a clinically relevant adjuvant that augments CAR-NK cell efficacy through dual mechanisms: metabolic enhancement of effector functions and protection against microenvironmental oxidative suppression, thereby offering a translatable strategy to improve CAR-NK therapy for ovarian cancer. - Source: PubMed
Publication date: 2026/08/13
Ouyang XinDeng XiaotongWang QizhaoChu MinghuiWei XinyuWang MengtingXiang ChunmingZhang PengSun ZheShen ShijunXu Yao - Mesothelin (MSLN) is a therapeutic target for antibody-drug conjugates (ADCs) due to its tumor-selective overexpression. However, soluble MSLN (sMSLN) in circulation compromises efficacy by acting as a decoy. RC88 is a clinical-stage ADC composed of a humanized anti-MSLN antibody conjugated to a monomethyl auristatin E (MMAE) payload. This study elucidates the unique binding mechanism that allows RC88 to maintain superior efficacy despite sMSLN interference. - Source: PubMed
Publication date: 2026/07/08
Xu YidanLi MingyangWang LiliWang KailinWang XiaoZhang XiaopingYu ZhanjiaoXin YinghaoHe ChenglinHe XiangyiZhou JingMin XiaoshanChen HangWang ZhulunLi DongFang JianminLi Yuanhao - Chimeric antigen receptor (CAR)-T cell therapy is largely ineffective in most solid tumors, partially because of inadequate intratumoral trafficking. Bridging therapy, administered between leukapheresis and CAR-T cell infusion, offers a distinct opportunity to control the disease and precondition the tumor microenvironment without directly exposing CAR-T cells to concomitant drugs. Here, a poly (ADP-ribose) polymerase (PARP) inhibitor combined with anlotinib is evaluated as bridging therapy for ovarian cancer. In immunocompetent mice bearing ovarian tumors, this regimen induces durable intratumoral T cell accumulation associated with activation of the cGAS-STING pathway, vascular normalization, and reduced fibrillar collagen deposition. Furthermore, TGFβ-resistant, dual-target mesothelin (MSLN)/CD19 CAR-T cells are engineered using a bait-and-switch strategy. Niraparib plus anlotinib administered as bridging therapy before CAR-T cell infusion enhances CAR-T cell infiltration and antitumor activity across multiple preclinical ovarian cancer models. These findings inform an ongoing phase I clinical trial (NCT05141253) evaluating the safety of these engineered CAR-T cells following bridging therapy in patients with refractory MSLN-positive solid tumors. Collectively, our findings support a clinically actionable bridging therapy with translational potential for potentiating CAR-T cell therapy in ovarian cancer and highlight bridging therapy as a translational approach to improve CAR-T cell access and efficacy in solid tumors. - Source: PubMed
Publication date: 2026/08/10
Li HuayiXiang MinghuaXu QiuyangLiu JiahaoJiao XiaofeiMu WeiLv XiaoyingTao KangjiaXu YuZhou DongchenGong WenjianYan DanmeiHu YixinXu SenZhao BingbingLi JundongGai YongkangHu GuangZhu LiGao QingleiFang Yong