Be0101

Manufactured by BioXCell

Sourced in United States

BE0101 is a laboratory centrifuge designed for general-purpose applications. It features a compact and user-friendly design, allowing for efficient separation of samples in a variety of scientific and research settings.

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Lab products found in correlation

39 protocols using be0101

Comprehensive Tumor Immunotherapy Protocol

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Female C57BL/6 mice aged 6–8 weeks were purchased from the Center of Experimental Animals of the Third Military Medical Univercity (TMMU). Nude mice were purchased from VitalStar Biotechnology Co. Ltd. (Beijing, China). The mouse handling protocols were approved by the Institutional Animal Care and Use Committee of TMMU. To establish tumor models, B16F10 cells (2 × 10⁵ in 100 µL of PBS) were subcutaneously inoculated into the right flank of 6–8-week-old female C57BL/6 mice or nude mice. When the tumors became palpable, tumor volume was monitored twice per week. In immunotherapeutic models, 2 × 10⁵ B16F10 cells were subcutaneously inoculated into the right flank of 6–8-week-old female C57BL/6 mice. Mice received 200 µg of intraperitoneal anti-PD-L1 monoclonal antibody (10F.9G2, Be0101, BioXcell) or the equivalent isotype control antibody (BioXcell, BE0090) on days 4, 7, and 10.
For radiation-combined immunotherapeutic models, 2 × 10⁵ B16F10 cells were subcutaneously inoculated into the right legs of C57BL/6 mice. When the tumors reached approximately 50 mm³, the mice were locally irradiated using the Varian Trilogy Stereotactic System at a single dose of 20 Gy. On the same day, 200 µg of anti-PD-1 monoclonal antibody (10F.9G2, Be0101, BioXcell) or equivalent isotype control antibody (BioXcell, BE0090) was injected intraperitoneally every three days three times.

Gong Z., Jia Q., Guo J., Li C., Xu S., Jin Z., Chu H., Wan Y.Y., Zhu B, & Zhou Y. (2023). Caspase-8 contributes to an immuno-hot microenvironment by promoting phagocytosis via an ecto-calreticulin-dependent mechanism. Experimental Hematology & Oncology, 12, 7.

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Systemic and Intratumoral Immunotherapy Protocols

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Treatment diagrams are provided for each specific experiment. APD-1 treatments consisted of systemically (intraperitoneally) delivered antibody dosed as 0.1 mg (clone 10F.9G2, BE0101, BioXCell, Lebanon, New Hampshire, USA) diluted in PBS. Virotherapy treatments consisted of 1 x 10⁸ viral particles (including equal amounts of Ad5-CMV-mIL2 and Ad5-CMV-mTNFa viruses, non-replicative in mice but historically used as model for the Ad5 man-based therapies which are replication competent in that host). The expression of TNFa and IL-2 after the use of the viruses in B16.OVA model has been studied before (23 (link)). In those experiments including intratumoral virus treatments, control groups not receiving viruses were injected intratumorally with an equivalent amount of PBS.

Cervera-Carrascon V., Quixabeira D.C., Santos J.M., Havunen R., Milenova I., Verhoeff J., Heiniö C., Zafar S., Garcia-Vallejo J.J., van Beusechem V.W., de Gruijl T.D., Kalervo A., Sorsa S., Kanerva A, & Hemminki A. (2021). Adenovirus Armed With TNFa and IL2 Added to aPD-1 Regimen Mediates Antitumor Efficacy in Tumors Refractory to aPD-1. Frontiers in Immunology, 12, 706517.

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Immune checkpoint inhibition and CCR2 blockade

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Anti-PD-L1 (1.5 mg; rat IgG2b isotype; clone 10F.9G2; BioXCell; BE0101) or isotype control (1.5 mg; anti-keyhole limpet hemocyanin; clone LTF-2; BioXCell; BE0090) antibodies were administered intraperitoneally (i.p.).
For CCR2 blockade, the anti-CCR2 monoclonal antibody MC21 [29 (link)], was injected i.p. (400 μg) every 4 days.

Ben-Yehuda H., Arad M., Peralta Ramos J.M., Sharon E., Castellani G., Ferrera S., Cahalon L., Colaiuta S.P., Salame T.M, & Schwartz M. (2021). Key role of the CCR2-CCL2 axis in disease modification in a mouse model of tauopathy. Molecular Neurodegeneration, 16, 39.

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Anti-CTLA-4 and Anti-PD-L1 Therapy in Murine Tumors

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Studies of anti–CTLA-4 (BE0032, Bio X Cell) and anti–PD-L1 (BE0101, Bio X Cell) therapy in mice bearing 4T1 and LLC tumors, as well as studies of scAAV monotherapy and combination treatment, are consistent with the descriptions above. The administration methods of each drug are shown in the respective flow charts in the figures.

Long Y., Chen R., Yu X., Tong Y., Peng X., Li F., Hu C., Sun J, & Gong L. (2022). Suppression of Tumor or Host Intrinsic CMTM6 Drives Antitumor Cytotoxicity in a PD-L1–Independent Manner. Cancer Immunology Research, 11(2), 241-260.

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Intratumoral Immunotherapy Combination

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To study treatment-induced changes in tumors, 2.5 × 10⁵ B16.OVA melanoma cells were implanted subcutaneously on 4–6 week old female C57BL/6JOlaHsd mice (Envigo Labs, Huntingdon, UK). Eleven days after engraftment, animals were randomized into groups (n = 12-14/group). Then, they received systemic treatments of 0.1 mg of anti-PD-L1 (clone 10 F.9G2, BE0101, BioXCell, Lebanon, New Hampshire, USA) and intratumoral injections of 1 × 10⁸ vp (including equal amounts of Ad5-CMV-mIL2 and Ad5-CMV-mTNFa viruses, non-replicative in mice) on days 0, 1, 3, and 6. PBS was injected intratumorally for groups that did not receive virus. On day 7, 6 animals per group were sacrificed and tumors collected to investigate immune-cell phenotyping and cytokine signatures. The rest of the animals (n = 6–8/group) continued to a 90-d OS study, where the treatments continued once every 3 d, until maximum tumor size reached (18 mm) or complete tumor regression.

Cervera-Carrascon V., Quixabeira D.C., Santos J.M., Havunen R., Zafar S., Hemminki O., Heiniö C., Munaro E., Siurala M., Sorsa S., Mirtti T., Järvinen P., Mildh M., Nisen H., Rannikko A., Anttila M., Kanerva A, & Hemminki A. (2020). Tumor microenvironment remodeling by an engineered oncolytic adenovirus results in improved outcome from PD-L1 inhibition. Oncoimmunology, 9(1), 1761229.

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Anti-CD70 and Anti-PD-L1 Therapy for Murine Lymphoma

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Female BALB/c mice were purchased from Guangdong Medical Lab Animal Center and housed in a specific pathogen‐free mouse facility. Murine A20 lymphoma cells³¹ (1×10⁶/100 μl), derived from BALB/c mice, were injected subcutaneously into the flank. When the tumour was palpable, cohorts of mice were intraperitoneally injected with IgG (BioXCell, BE0090), 300 μg of anti‐CD70 (BioXCell, BE0022), 200 μg of anti‐PD‐L1 (BioXCell, BE0101), or a combination of these antibodies every 3 days for a total of 4 times. Tumour growth was evaluated by measuring the tumour volume every 3 days. When the mice were sacrificed, the tumours were harvested for further investigation. The institutional animal care and use committee of Sun Yat‐Sen University approved the study.

Nie M., Ren W., Ye X., Berglund M., Wang X., Fjordén K., Du L., Giannoula Y., Lei D., Su W., Li W., Liu D., Linderoth J., Jiang C., Bao H., Jiang W., Huang H., Hou Y., Zhu S., Enblad G., Jerkeman M., Wu K., Zhang H., Amini R., Li Z, & Pan‐Hammarström Q. (2022). The dual role of CD70 in B‐cell lymphomagenesis. Clinical and Translational Medicine, 12(12), e1118.

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Murine Tumor Immunotherapy Evaluation

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B16F10-gp33 (3 × 10⁵) cells or E.G7-Ova (4 × 10⁵) cells resuspended in 100 µL PBS were subcutaneously injected into the shaved left flanks of mice between the ages of 8 to 16 weeks. Tumor growth was tracked every 3 days using a caliper. On day 10 after inoculation, mice bearing tumors of approximately 5-mm diameter were randomly distributed to each group for intravenous (i.v.) infusion of 1×10⁶ T cells. Mice with ulceration/necrosis or tumors over 225 mm² were euthanized and recorded as deceased. For in vivo depletion of Tregs, FoxP3⁺ cells were transiently ablated in DEREG mice, which are mice in which DTR-eGFP is selectively expressed under the direct control of the FoxP3 promoter. FoxP3⁺ cells were depleted by intraperitoneal (i.p.) administration of 10 ng per g body weight diphtheria toxin (Merck) on days 10, 11, 19, and 20 after tumor inoculation. For CD8⁺ T-cell depletion, monoclonal antibodies were prepared in-house using the CD8 hybridoma cells (YTS169), which were acquired from Dr. Rolf M. Zinkernagel (University of Zurich), and CellMax artificial capillary cell culture systems. For experiments involving PD-L1 blockade, 100 µg of anti–PD-L1 (catalog no. BE0101, Bio X Cell) or rat IgG2b isotype control (catalog no. BE0090, Bio X Cell) were i.p. injected on days 10, 14, and 18 after tumor inoculation.

Han S., Liu Z.Q., Chung D.C., Paul M.S., Garcia-Batres C.R., Sayad A., Elford A.R., Gold M.J., Grimshaw N, & Ohashi P.S. (2022). Overproduction of IFNγ by Cbl-b–Deficient CD8+ T Cells Provides Resistance against Regulatory T Cells and Induces Potent Antitumor Immunity. Cancer Immunology Research, 10(4), 437-452.

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Tumor Regression with Immune Checkpoint Blockade

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3 × 10⁶ U14 cells were subcutaneously injected as described above. Seven days post tumor cell injection, anti-PD-L1 antibody [In vivo mab anti-mouse PD-L1 (B7-H1), BioX Cell, BE0101] and anti-CD25 (IL-2Rα, In vivo plus anti-mouse CD25, BioX Cell, BP0012) were intraperitoneally injected (200 μg per dose per mouse) as indicated schedule. Mice were euthanized and tumors were harvested after five times’ antibody injections. The resected tumors were photographed and measured.

Xu F., Zhang F., Wang Q., Xu Y., Xu S., Zhang C, & Wang L. (2021). The augment of regulatory T cells undermines the efficacy of anti-PD-L1 treatment in cervical cancer. BMC Immunology, 22, 60.

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Immunotherapy combinations in mice

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One week after intrasplenic injection, mice received (a) rat IgG2b isotype antibody (Bioxcell BE0090) and vehicle (0.5% HPMC/0.1% Tween-80) (n = 6), (b) ALK5i and isotype antibody (n = 6), (c) anti-PD-L1 antibody (Bioxcell BE0101) and vehicle (n = 6), or (d) combination of ALK5i and anti-PD-L1 antibody (n = 6). Anti-PD-L1 and isotype antibody were injected at 10 mg/kg intraperitoneal (IP) twice per week. After 3 weeks, mice were euthanized and tissues were collected for analysis.

Nair R., Lannagan T.R., Jackstadt R., Andrusaite A., Cole J., Boyne C., Nibbs R.J., Sansom O.J, & Milling S. (2024). Co-inhibition of TGF-β and PD-L1 pathways in a metastatic colorectal cancer mouse model triggers interferon responses, innate cells and T cells, alongside metabolic changes and tumor resistance. Oncoimmunology, 13(1), 2330194.

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Evaluating Atad3a Knockdown and Immunotherapy in Murine Breast Cancer

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Animal experiments were approved by the Institutional Animal Care and Use Committee at Army Medical University (AMUWEC20201344). For the immunodeficiency mouse model, 4T1 tumors formed by control or Atad3a-knockdown cells (1 × 10⁵ cells in 50 μL PBS mixed with 50 μL Matrigel, Corning) were injected into the fourth left mammary fat pads of female BALB/c nude mice. For the immune-competent mouse model, 4T1 tumors formed by control or Atad3a-knockdown cells (5 × 10⁴ cells in 50 μL PBS mixed with 50 μL Matrigel, Corning) were injected into the fourth left mammary fat pads of female BALB/c mice. For in vivo treatment, mice were treated randomly with paclitaxel (8 mg/kg, HY-B0015, MedChemExpress) or vehicle intraperitoneally on 5, 8, 11, and 14 days after tumor cells inoculation, while mouse anti-PD-L1 antibody (100 μg per mouse, clone 10 F.9G2, BE0101, BioXcell) or rat IgG2b isotype control (100 μg per mouse, clone LTF-2, BE0090, BioXcell) was utilized on 6, 9, 12, 15 days after inoculation. Orthotropic tumor sizes were measured every 4 days with a caliper and tumor volumes = Length × Width²/2 were calculated.

Xie X.Q., Yang Y., Wang Q., Liu H.F., Fang X.Y., Li C.L., Jiang Y.Z., Wang S., Zhao H.Y., Miao J.Y., Ding S.S., Liu X.D., Yao X.H., Yang W.T., Jiang J., Shao Z.M., Jin G, & Bian X.W. (2023). Targeting ATAD3A-PINK1-mitophagy axis overcomes chemoimmunotherapy resistance by redirecting PD-L1 to mitochondria. Cell Research, 33(3), 215-228.

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