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#36472839   // To Up

Nemvaleukin alfa, a novel engineered IL-2 fusion protein, drives antitumor immunity and inhibits tumor growth in small cell lung cancer.

Small cell lung cancer (SCLC) is a deadly disease with a 5-year survival of less than 7%. The addition of immunotherapy to chemotherapy was recently approved as first-line treatment; however, the improved clinical benefit is modest, highlighting an urgent need for new treatment strategies. Nemvaleukin alfa, a novel engineered interleukin-2 fusion protein currently in phase I-III studies, is designed to selectively expand cytotoxic natural killer (NK) cells and CD8 T cells. Here, using a novel SCLC murine model, we investigated the effects of a mouse version of nemvaleukin (mNemvaleukin) on tumor growth and antitumor immunity.
Yuanwang Pan, Yuan Hao, Han Han, Ting Chen, Hailin Ding, Kristen E Labbe, Elaine Shum, Kayla Guidry, Hai Hu, Fiona Sherman, Ke Geng, Janaye Stephens, Alison Chafitz, Sittinon Tang, Hsin-Yi Huang, Chengwei Peng, Christina Almonte, Jared E Lopes, Heather C Losey, Raymond J Winquist, Vamsidhar Velcheti, Hua Zhang, Kwok-Kin Wong

1356 related Products with: Nemvaleukin alfa, a novel engineered IL-2 fusion protein, drives antitumor immunity and inhibits tumor growth in small cell lung cancer.

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#36472428   2022/12/06 To Up

Synergistic Antibacterial Effect and Mechanism of Allicin and an Enterobacter cloacae Bacteriophage.

Enterobacter cloacae is a troublesome pathogen causing refractory infections of the lower respiratory tract, urethra and abdominal cavity, endocarditis, osteomyelitis, and neonatal septicemia. It is prone to developing resistance to ordinary antibiotics and has brought a serious problem to clinical treatment. An artful synergistic combination of an antibacterial natural product allicin and a newly isolated bacteriophage, named BD523, was constructed herein. This combination significantly lowered effective dosage of allicin and effectually overcame bacterial drug-resistance. We experimentally evidenced that allicin interacts with bacterial DNA in the groove region by inserting itself into the DNA double helix and, subsequently, disrupts the bacterial DNA by cleaving phosphate diester bonds of deoxynucleotides. Further, BD523 destroys the cell wall and membrane of bacteria by synthesizing lyase proteins, including holin and endolysins. Thus, the synergistic effect of the combination benefits from complementary targeting mechanisms of allicin and BD523. They cooperatively act on bacterial DNA, cell wall, and membrane to improve antibacterial efficiency and avoid drug-resistance. Bacterial drug-resistance is a serious problem afflicting pharmacologists all over the world. Many strategies have been developed and practiced to overcome it, but almost no one is satisfactory due to the continual change of bacteria. Combinations of antibiotics and bacteriophages are promising because of the cooperation of 2 bacterial killers with distinct mechanisms. The combination of allicin and an Enterobacter cloacae bacteriophage reported herein can significantly improve the effect of allicin against E. cloacae. Its synergistic effect was even superior to the combination of bacteriophage and neomycin, of which the MIC was significantly lower than allicin. It was ascribed to the complementary antibacterial and the possible resistance-proof mechanism of bacteriophage and allicin. This study provided a pragmatic way to conquer the cunning bacterium, and may offer reference for research and development of new bacterial killers.
Zhi Tao, Di Geng, Jiayue Tao, Jing Wang, Siqi Liu, Qiaoxia Wang, Feng Xu, Shengyuan Xiao, Rufeng Wang

2071 related Products with: Synergistic Antibacterial Effect and Mechanism of Allicin and an Enterobacter cloacae Bacteriophage.

5mg25 mg200 100ug 5 G 5 G100ug1 g1000 TESTS/0.65ml100ul96 wells (1 kit)200ul

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#36471724   2022/12/01 To Up

Nanoformulations targeting immune cells for cancer therapy: mRNA therapeutics.

The approved worldwide use of two messenger RNA (mRNA) vaccines (BNT162b2 and mRNA-1273) in late 2020 has proven the remarkable success of mRNA therapeutics together with lipid nanoformulation technology in protecting people against coronaviruses during COVID-19 pandemic. This unprecedented and exciting dual strategy with nanoformulations and mRNA therapeutics in play is believed to be a promising paradigm in targeted cancer immunotherapy in future. Recent advances in nanoformulation technologies play a prominent role in adapting mRNA platform in cancer treatment. In this review, we introduce the biologic principles and advancements of mRNA technology, and chemistry fundamentals of intriguing mRNA delivery nanoformulations. We discuss the latest promising nano-mRNA therapeutics for enhanced cancer immunotherapy by modulation of targeted specific subtypes of immune cells, such as dendritic cells (DCs) at peripheral lymphoid organs for initiating mRNA cancer vaccine-mediated antigen specific immunotherapy, and DCs, natural killer (NK) cells, cytotoxic T cells, or multiple immunosuppressive immune cells at tumor microenvironment (TME) for reversing immune evasion. We highlight the clinical progress of advanced nano-mRNA therapeutics in targeted cancer therapy and provide our perspectives on future directions of this transformative integrated technology toward clinical implementation.
Wei Yang, Jianwei Cao, Hui Cheng, Liang Chen, Meihua Yu, Yu Chen, Xingang Cui

2154 related Products with: Nanoformulations targeting immune cells for cancer therapy: mRNA therapeutics.

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#36471484   // To Up

Single-cell transcriptomic analysis of PB and BM NK cells from severe aplastic anaemia patients.


Chunyan Liu, Yingying Chen, Dan Lu, Bingnan Liu, Tian Zhang, Ling Deng, Zixuan Liu, Congwei Zhong, Rong Fu

1675 related Products with: Single-cell transcriptomic analysis of PB and BM NK cells from severe aplastic anaemia patients.

100 µg1.00 flaskOne Vial: 5 X 10^6 Cells100ml1.5x10(6) cells10ml100 µg101 Unit

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#36470338   2022/12/02 To Up

T cell senescence: A crucial player in autoimmune diseases.

Senescent T cells are terminally differentiated, proliferative, and disabled lymphocytes that lack an antigen-specific response. The development of T-cell senescence in autoimmune diseases contributes to immunological disorders and disease progression. Senescent T cells lack costimulatory markers and reduce the T cell receptor (TCR) repertoire and the uptake of natural killer cell receptors. Senescent T cells exert cytotoxic effects through the expression of perforin, granzymes, tumor necrosis factor (TNF), and other cytokines without the antigen-presenting process. DNA accumulation, telomere damage, and limited DNA repair capacity are important features of senescent T cells. Impaired mitochondrial function and accumulation of reactive oxygen species (ROS) are also observed. Alleviation of T cell senescence could provide potential targets for the treatment of autoimmune diseases.
Yinyun Lu, Yongchun Ruan, Pan Hong, Qi Liu, Ke Rui, Shengjun Wang, Dawei Cui

1110 related Products with: T cell senescence: A crucial player in autoimmune diseases.

500 tests96 tests500 tests

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#36470166   2022/11/21 To Up

Sleep disturbance is associated with perturbations in immune-inflammatory pathways in oncology outpatients undergoing chemotherapy.

Sleep disturbance is a common problem in patients receiving chemotherapy. Purpose was to evaluate for perturbations in immune-inflammatory pathways between oncology patients with low versus very high levels of sleep disturbance.
Alejandra Calvo-Schimmel, Kord M Kober, Steven M Paul, Bruce A Cooper, Carolyn Harris, Joosun Shin, Marilyn J Hammer, Yvette P Conley, Vasuda Dokiparthi, Adam Olshen, Jon D Levine, Christine Miaskowski

1186 related Products with: Sleep disturbance is associated with perturbations in immune-inflammatory pathways in oncology outpatients undergoing chemotherapy.

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#36468334   2022/12/05 To Up

Repeated lipoprotein apheresis and immune response: Effects on different immune cell populations.

Atherosclerosis is considered a chronic inflammation of arterial vessels with the involvement of several immune cells causing severe cardiovascular diseases. Lipoprotein apheresis (LA) improves cardiovascular conditions of patients with severely disturbed lipid metabolism. In this context, little is known about the impact of LA on various immune cell populations, especially over time.
Romy Walther, Rebekka Wehner, Antje Tunger, Ulrich Julius, Ulrike Schatz, Sergey Tselmin, Stefan R Bornstein, Marc Schmitz, Juergen Graessler

2013 related Products with: Repeated lipoprotein apheresis and immune response: Effects on different immune cell populations.

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#36468038   2022/11/21 To Up

Construction of a mitochondrial dysfunction related signature of diagnosed model to obstructive sleep apnea.

The molecular mechanisms underlying obstructive sleep apnea (OSA) and its comorbidities may involve mitochondrial dysfunction. However, very little is known about the relationships between mitochondrial dysfunction-related genes and OSA. Mitochondrial dysfunction-related differentially expressed genes (DEGs) between OSA and control adipose tissue samples were identified using data from the Gene Expression Omnibus database and information on mitochondrial dysfunction-related genes from the GeneCards database. A mitochondrial dysfunction-related signature of diagnostic model was established using least absolute shrinkage and selection operator Cox regression and then verified. Additionally, consensus clustering algorithms were used to conduct an unsupervised cluster analysis. A protein-protein interaction network of the DEGs between the mitochondrial dysfunction-related clusters was constructed using STRING database and the hub genes were identified. Functional analyses, including Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, gene set enrichment analysis (GSEA), and gene set variation analysis (GSVA), were conducted to explore the mechanisms involved in mitochondrial dysfunction in OSA. Immune cell infiltration analyses were conducted using CIBERSORT and single-sample GSEA (ssGSEA). we established mitochondrial dysfunction related four-gene signature of diagnostic model consisted of , and which could easily distinguish between OSA patients and controls. In addition, based on mitochondrial dysfunction-related gene expression, we identified two clusters among all the samples and three clusters among the OSA samples. A total of 10 hub genes were selected from the PPI network of DEGs between the two mitochondrial dysfunction-related clusters. There were correlations between the 10 hub genes and the 4 diagnostic genes. Enrichment analyses suggested that autophagy, inflammation pathways, and immune pathways are crucial in mitochondrial dysfunction in OSA. Plasma cells and M0 and M1 macrophages were significantly different between the OSA and control samples, while several immune cell types, especially T cells (γ/δ T cells, natural killer T cells, regulatory T cells, and type 17 T helper cells), were significantly different among mitochondrial dysfunction-related clusters of OSA samples. A novel mitochondrial dysfunction-related four-gen signature of diagnostic model was built. The genes are potential biomarkers for OSA and may play important roles in the development of OSA complications.
Qian Liu, Tao Hao, Lei Li, Daqi Huang, Ze Lin, Yipeng Fang, Dong Wang, Xin Zhang

2070 related Products with: Construction of a mitochondrial dysfunction related signature of diagnosed model to obstructive sleep apnea.

1 kit(96 Wells)1 ml100 1 module100 ug 100ul100 assays1 mL1 g100 μg1 mL1 module

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#36467789   2022/10/13 To Up

Aggressive, early resistant and relapsed mantle cell lymphoma distinct extrinsic microenvironment highlighted by transcriptome analysis.

Immunotherapy strategies relying on innate or adaptive immune components are increasingly used in onco-haematology. However, little is known about the infiltrated lymph nodes (LN) or bone marrow (BM) landscape of mantle cell lymphoma (MCL). The original transcriptomic approach of reverse transcriptase multiplex ligation-dependent probe amplification (RT-MLPA) was applied here to explore the expression of 24 genes of interest in MCL at diagnosis (21 LN and 15 BM) or relapse (18 LN). This allowed us to identify that at baseline, samples from MCL patients with an aggressive morphology (i.e. blastoid or pleomorphic) or a high proliferative profile, displayed significantly higher monocyte/macrophage-associated transcripts ( and in LN and BM. Regarding T-cells, aggressive MCL forms had significantly lower amounts of LN transcripts, yet an increased expression of cytotoxic markers in LN () and BM (). A very high-risk group with early treatment resistance displayed, at diagnosis, high proliferation () and high macrophages and cytotoxic transcript levels. Post-immunochemotherapy relapsed samples revealed lower levels of T- and natural killer-cells markers, while monocyte/macrophage markers remained similar to diagnosis. This study suggests that rapid analysis of MCL microenvironment transcriptome signatures by RT-MLPA could allow for an early distinction of patient subgroups candidates for adapted treatment strategies.
Yannick Le Bris, Adeline Normand, Louise Bouard, Audrey Ménard, Céline Bossard, Anne Moreau, Marie C Béné

1000 related Products with: Aggressive, early resistant and relapsed mantle cell lymphoma distinct extrinsic microenvironment highlighted by transcriptome analysis.

50 ml Ready-to-use 25 ml Ready-to-use 0.1ml (1mg/ml) 2 ml 6 ml Ready-to-use 96T

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#36467776   2022/11/30 To Up

Identification and Characterization of a Novel Dual Inhibitor of Indoleamine 2,3-dioxygenase 1 and Tryptophan 2,3-dioxygenase.

Kynurenine (Kyn), a metabolite of tryptophan (Trp), is a key regulator of mammal immune responses such as cancer immune tolerance. Indoleamine-2,3-dioxygenase (IDO) and tryptophan-2,3-dioxygenase (TDO) are main enzymes regulating the first and rate-limiting step of the Kyn pathway. To identify new small molecule inhibitors of TDO, we selected A172 glioblastoma cell line constitutively expressed TDO. Characterization of this cell line using kinase inhibitor library resulted in identification of MEK/ERK pathway-dependent TDO expression. After knowing the properties for TDO expression, we further proceeded to screen chemical library for TDO inhibitors. We previously determined that S-benzylisothiourea derivatives are enzymatic inhibitors of indoleamine 2,3-dioxygenase 1 (IDO1) and suggested that the isothiourea moiety could be an important pharmacophore for binding to heme. Based on this premise, we screened an in-house library composed of various isothiourea derivatives and identified a bisisothiourea derivative, PVZB3001, as an inhibitor of TDO. Interestingly, PVZB3001 also inhibited the enzymatic activity of IDO1 in both cell-based and cell-free assays but did not inhibit other heme enzymes. Molecular docking studies suggested the importance of isothiourea moieties at the ortho position of the phenyl ring for the inhibition of catalytic activity. PVZB3001 showed competitive inhibition against TDO, and this was supported by the docking simulation. PVZB3001 recovered natural killer (NK) cell viability and functions by inhibiting Kyn accumulation in conditioned medium of both IDO1- and TDO-expressing cells. Furthermore, oral administration of IDO1-overexpressing tumor-bearing mice with PVZB3001 significantly inhibited tumor growth. Thus, we identified a novel selective dual inhibitor of IDO1 and TDO using the Kyn production assay with a glioblastoma cell line. This inhibitor could be a useful pharmacological tool for modulating the Kyn pathway in a variety of experimental systems.
Saeko Yoshioka, Tomonori Ikeda, Sogo Fukuchi, Yurika Kawai, Katsumi Ohta, Hisashi Murakami, Naohisa Ogo, Daisuke Muraoka, Osamu Takikawa, Akira Asai

1461 related Products with: Identification and Characterization of a Novel Dual Inhibitor of Indoleamine 2,3-dioxygenase 1 and Tryptophan 2,3-dioxygenase.

100ug10 mg1000 tests100 mg1000 100ug0.1 ml100ug25 mg2.5 mg1000 TESTS/0.65ml100ug

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