Syrian hamster igg

Manufactured by BioXCell

Sourced in United States

Syrian hamster IgG is an antibody protein produced by the immune system of Syrian hamsters. It is commonly used in research applications as a reagent or control in laboratory experiments.

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Lab products found in correlation

Rat igg2a, by BioXCell (2 mentions) Cyclophosphamide, by Merck Group (1 mentions) αctla 4 clone 9h10, by BioXCell (1 mentions) Rmp1 14, by BioXCell (1 mentions) Rat anti mouse pd l1, by BioXCell (1 mentions) Rat igg2b, by BioXCell (1 mentions) Anti ctla4 9h10, by BioXCell (1 mentions) Be0131, by BioXCell (1 mentions) Poly 1 c adjuvant, by InvivoGen (1 mentions) Be0031, by BioXCell (1 mentions)

6 protocols using syrian hamster igg

Checkpoint Blockade and Chemotherapy

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Checkpoint blockade therapy consisting on a combination of 200 μg of αCTLA-4 (clone 9H10, BioXCell) and 200 μg of αPD-1 (RMP1-14, BioXCell) antibodies per dose or isotype control antibodies (Syrian hamster IgG and Rat IgG2a, respectively, BioXCell) was administered on days 5, 7 and 9 after tumor injection, which consisted on 0.5x10⁶ MC38 colon carcinoma cells injected subcutaneously.
The treatment with chemotherapy was administered on days 5, 7 and 9 after the subcutaneous injection of 0.5x10⁶ LLC tumor cells. Cyclophosphamide (i.p., 170mg/kg) was purchased from Sigma.

Palazon A., Tyrakis P.A., Macias D., Veliça P., Rundqvist H., Fitzpatrick S., Vojnovic N., Phan A.T., Loman N., Hedenfalk I., Hatschek T., Lövrot J., Foukakis T., Goldrath A.W., Bergh J, & Johnson R.S. (2017). An HIF-1α/VEGF-A Axis in Cytotoxic T Cells Regulates Tumor Progression. Cancer Cell, 32(5), 669-683.e5.

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Modulating Tumor Immunity via CTLA4 and PD-L1

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8- to 12-week-old female mice were injected subcutaneously with 100μl PBS containing 5×10⁵ B16ova melanoma cells into the left, ventral flank. Intraperitoneal injection of 200μl PBS containing either 0.4mg of a Syrian hamster anti-mouse CTLA4 (Clone UC10-4F10-11; BE0131), 0.5mg rat anti-mouse PD-L1 (Clone10F.9G2; BE0101), 0.4mg Syrian hamster IgG (BE0087) or 0.5mg rat IgG2b (Clone LTF-2; BE0090) (all from BioXCell, USA) was performed every 3 days starting from day 0 of B16ova challenge until day 18.
Tumor volume was calculated according to the following equation: V = π/6*length*width². For survival analysis, mice with tumors exceeding the length limit of 15 mm were sacrificed and counted as dead.

Peer S., Baier G, & Gruber T. (2017). Cblb-deficient T cells are less susceptible to PD-L1-mediated inhibition. Oncotarget, 8(26), 41841-41853.

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Pan02 Subcutaneous Tumor Model with ST-SOT and ICB

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For the Pan02 subcutaneous tumor model, tumors were allowed to grow for two weeks until reaching an average volume of 100 mm³. At this time, all mice were treated with 2.5 × 10⁶ CFU ST-SOT intravenously two days in a row. Three days after the first treatment, mice were randomized into four groups: (1) ST-SOT uninduced + IgG (n = 3), (2) ST-SOT uninduced + ICB (n = 4), (3) ST-SOT induced + IgG (n = 4), and (4) ST-SOT induced + ICB (n = 4). Induced groups received 250 mg L-Arabinose via intraperitoneal injection while uninduced groups received an equivalent volume of PBS. IgG groups received 200 µg Armenian Hamster IgG with 75 µg Syrian Hamster IgG (BioXCell; Lebanon, NH, USA) and ICB groups received 200 µg anti-PD-1 (J43) (gift from Dr. Blazar) with 75 µg anti-CTLA-4 (9H10) (BioXCell; Lebanon, NH, USA). Maintenance doses of IgG or ICB were given at reduced amounts (100 µg anti-PD-1/IgG and 40 µg anti-CTLA-4/IgG) every 3 days until the end of the experiment. Tumor volumes were measured thrice weekly using digital calipers. Tumor growth is represented as fold change in growth compared to volume at initial ST-SOT treatment.

Ebelt N.D., Zamloot V., Zuniga E., Passi K.B., Sobocinski L.J., Young C.A., Blazar B.R, & Manuel E.R. (2021). Collagenase-Expressing Salmonella Targets Major Collagens in Pancreatic Cancer Leading to Reductions in Immunosuppressive Subsets and Tumor Growth. Cancers, 13(14), 3565.

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VH1-2 rearranging germline mouse model

Cited 1 time

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Mice expressing the VH1-2 rearranging germline and the rearranged gl-VRC01 light chain were engineered as previously described^{45 (link)}, with the additional substitution of mouse J_H1-4 with human J_H2 segment^{45 (link)}. For immunization studies, mice were immunized sequentially with 25 µg of protein per animal in 60 µg of Poly I:C adjuvant (Invivogen) at two sites intramuscularly. For antibody coadministration 250 µg of anti-CTLA-4(BioXCell #BE0131), anti-OX-40 (BioXCell #BE0031) or a combination of isotype controls (Syrian Hamster IgG (BioXCell #BE0087) + Rat IgG2a (BioXCell #BE0089)). Mice were harvested at week 11 and spleen, lymph node and blood were isolated. All mice used in this study were housed in the Medical Sciences Research Building II Vivarium at Duke University Medical center in a pathogen-free environment with 12-h light/datk cycles at 20–25 ˚C, in accordance with Duke University Institutional Animal Care and Use Committee-approved animal protocols. All aspects of the procurement, conditioning/quarantine, housing, colony management, veterinary care, and carcass disposal programs comply with the guidelines set forth by the NIH guide for the care and use of laboratory animals, the Animal Welfare Act, and all applicable federal, state and institutional laws.

Bradley T., Kuraoka M., Yeh C.H., Tian M., Chen H., Cain D.W., Chen X., Cheng C., Ellebedy A.H., Parks R., Barr M., Sutherland L.L., Scearce R.M., Bowman C.M., Bouton-Verville H., Santra S., Wiehe K., Lewis M.G., Ogbe A., Borrow P., Montefiori D., Bonsignori M., Anthony Moody M., Verkoczy L., Saunders K.O., Ahmed R., Mascola J.R., Kelsoe G., Alt F.W, & Haynes B.F. (2020). Immune checkpoint modulation enhances HIV-1 antibody induction. Nature Communications, 11, 948.

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Clodronate Liposomes and Anti-PDPN Antibody Treatment

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250 μL of PBS- or clodronate-liposomes (ClodronateLiposomes. com) was administered intravenous (i.v.) at 1 d.p.s.t. (day 7 analysis) or 1 and 7 d.p.s.t. (day 15 analysis). Anti-podoplanin (PDPN) antibody (clone 8.1.1) or Syrian Hamster IgG (both from BioXcell) was administered i.v. 3, 7, and 10 d.p.s.t. at 125 μg/dose.

McCabe A., Smith J.N., Costello A., Maloney J., Katikaneni D, & MacNamara K.C. (2018). Hematopoietic stem cell loss and hematopoietic failure in severe aplastic anemia is driven by macrophages and aberrant podoplanin expression. Haematologica, 103(9), 1451-1461.

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Orthotopic Glioblastoma Mouse Model with Immunotherapies

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C57BL/6 or athymic mice (7–8 weeks old) were obtained from the National Cancer Institute (Frederick, MD). All mouse procedures were approved by the Institutional Animal Care and Use Committee at the Massachusetts General Hospital. Dissociated 005 GSCs (2 × 10⁴ cells) or MGG123 GSCs (5 × 10³ cells) in 3 µl of their respective media were implanted stereotaxically into the striatum (2.2-mm lateral from Bregma and 2.5-mm deep) to generate orthotopic intracranial tumors. On indicated days after tumor implantation, mice were randomly divided into groups, intratumorally injected once or twice with G47Δ-mIL12 (as indicated) or PBS in 2 µl at the same stereotaxic coordinates, and/or injected intraperitoneally with axitinib (25 or 50 mg/kg; dissolved in polyethylene glycol 400 and acidified water, pH adjusted to 2.5–3) or vehicle solution for 1–3 cycles (1 cycle = 5 days on and 2 days off). Immune checkpoint inhibitor anti-mCTLA-4 antibodies (Syrian hamster clone 9H10; 5 mg/kg) or isotype control antibodies (Syrian hamster IgG) were obtained from BioXcell and administered 3-times intraperitoneally on indicated days after tumor implantation. Mice were followed for neurological symptoms and euthanized before becoming moribund. Animal caretakers were blinded to the treatment. Presence of tumor at sacrifice was evaluated macroscopically or after histological staining of sections.

Saha D., Wakimoto H., Peters C., Antoszczyk S.J., Rabkin S.D, & Martuza R.L. (2018). Combinatorial effects of VEGFR kinase inhibitor axitinib and oncolytic virotherapy in mouse and human glioblastoma stem-like cell models. Clinical cancer research : an official journal of the American Association for Cancer Research, 24(14), 3409-3422.

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