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Anti pd 1 antibody clone rmp1 14

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The Anti-PD-1 antibody (clone RMP1-14) is a laboratory reagent used in research applications. It binds to the Programmed Cell Death-1 (PD-1) receptor, which is an important immune checkpoint molecule involved in the regulation of T-cell activity. The antibody can be used in various immunological assays and experiments to study the role of PD-1 in immune system function.

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Lab products found in correlation

Nod shiltj mice, by Jackson ImmunoResearch (2 mentions) Rat igg2a isotype control, by BioXCell (1 mentions) Mouse tumor dissociation kit, by Miltenyi Biotec (1 mentions) Control antibody clone 2a3, by BioXCell (1 mentions) Ctla4 ig, by BioXCell (1 mentions) Gm csf, by Thermo Fisher Scientific (1 mentions) C57bl 6 mice, by Jackson ImmunoResearch (1 mentions) Anti cd8α clone 53 6.7, by BioXCell (1 mentions) Rat igg2a, by BioXCell (1 mentions) Basement membrane extract, by Bio-Techne (1 mentions) Isotype control antibodies clone 2a3, by BioXCell (1 mentions)

Close spelling variants of this product

Anti-mouse PD-1 antibody (clone RMP1-14) Anti-PD-1 monoclonal antibody (clone RMP1-14, PD-1 antibody (clone RMP1–14, Anti-PD-1 (clone RMP1-14, Anti-PD-1 antibody (RMP1–14) Clone RMP1-14 RMP1-14 Anti-PD-1 antibody PD-1 antibody Anti-PD-1

17 protocols using anti pd 1 antibody clone rmp1 14

1

Immune Checkpoint Blockade in PyMT Mice

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Mice expressing the polyoma virus middle T oncoprotein (PyMT) under the Mouse Mammary Tumor Virus (MMTV) promoter in a C57BL/6 background were used. In the PyMT model, the expression of the PyMT oncoprotein is restricted to the mammary epithelium, which results in the appearance of mammary tumors starting from 6 weeks after birth in C57BL/6 mice and the occurrence of pulmonary metastases starting after 18 weeks [35 (link)]. For analysis of immune checkpoint receptor expression, tumor bearing PyMT mice were sacrificed 18 weeks after birth, perfused with PBS and tumors were harvested for downstream applications. For immune checkpoint blockade in a therapeutic setting, animals were either treated with 5 mg/kg anti-BTLA antibody (clone 4G12b, produced as described before [34 (link)]), anti-PD-1 antibody (clone RMP1-14) or a rat IgG2a isotype control (both from BioXCell) once the first mammary tumor reached a size of 0.5 cm in diameter. Treatment with the antibodies was performed twice weekly for three weeks in regular intervals. Afterwards, animals were perfused and PyMT tumors and lungs were harvested for downstream applications. For all animal experiments the guidelines of the Hessian animal care and use committee were followed.
Sekar D., Govene L., del Río M.L., Sirait-Fischer E., Fink A.F., Brüne B., Rodriguez-Barbosa J.I, & Weigert A. (2018). Downregulation of BTLA on NKT Cells Promotes Tumor Immune Control in a Mouse Model of Mammary Carcinoma. International Journal of Molecular Sciences, 19(3), 752.
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2

Combination Therapy for Breast Cancer Mice

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Female C57BL/6 mice (six to eight weeks old) were obtained from Charles River Lab (Quebec, Canada) and kept at an ARD facility of the RI-MUHC. Mice were injected orthotopically with 2 × 105 Eo771 cells at m.f.p to form tumors. The animals were randomized into the four treatment groups, including control (isotype matched IgG2a and PBS), SAM (Life Science Laboratories, Lakewood, NJ, USA), anti-PD-1 antibody (clone RMP1-14, BioXcell, Lebanon, NH, USA), and SAM+anti-PD-1 combination. SAM (80 mg/kg) was diluted in PBS (1×) and was given daily using feeding needles via oral gavage once the tumors became palpable, and anti-PD-1 antibody (5 mg/kg) and isotype matched IgG2a antibody (5 mg/kg) were administered via intra-peritoneal (i.p.) injection twice a week. The dose of SAM and anti-PD-1 antibody was established previously [13 (link),28 (link),48 (link),77 (link),78 (link),79 (link)]. Tumor volume (T.V) was measured by palpation at timed intervals using a digital caliper. On day 20, the mice were sacrificed and tumor weight and T.V were measured. T.V was calculated using the formula T.V = (length × width2)/2. Percentage (%) tumor growth inhibition was calculated as ((1–[changes of T.V in treatment group/changes of T.V in control group] × 100). The mice were observed regularly for weight loss or potential adverse effects [80 (link)].
Mehdi A., Attias M., Arakelian A., Piccirillo C.A., Szyf M, & Rabbani S.A. (2022). Co-Targeting Luminal B Breast Cancer with S-Adenosylmethionine and Immune Checkpoint Inhibitor Reduces Primary Tumor Growth and Progression, and Metastasis to Lungs and Bone. Cancers, 15(1), 48.
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3

Passaging MC38 Tumor Models in Mice

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C57BL/6J mice bearing MC38 tumors were treated with 5 mg/kg anti-PD-1 antibody (clone RMP1-14, BioXCell, West Lebanon, NH, USA) or control antibody (clone 2A3, BioXCell) twice weekly by intraperitoneal (i.p.) injection. Tumors selected for passaging were excised, dissociated using a mouse tumor dissociation kit (Miltenyi Biotec, Bergisch Gladbach, Germany) and cultured in vitro until implantation into naïve mice. This process was repeated for a total of three rounds of passaging, with anti-PD-1 antibody dose increased to 10 mg/kg for the second and third rounds.
Bernardo M., Tolstykh T., Zhang Y.A., Bangari D.S., Cao H., Heyl K.A., Lee J.S., Malkova N.V., Malley K., Marquez E., Pollard J., Qu H., Roberts E., Ryan S., Singh K., Sun F., Wang E., Bahjat K., Wiederschain D, & Wagenaar T.R. (2021). An experimental model of anti-PD-1 resistance exhibits activation of TGFß and Notch pathways and is sensitive to local mRNA immunotherapy. Oncoimmunology, 10(1), 1881268.
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4

Immunotherapy Delays Type 1 Diabetes

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8-week-old female NOD/ShiLtJ mice (the Jackson Laboratory) were treated i.p. with either 200 μL of PBS (control group and PBS) or 8.2 μg (1.5 μg IL-2 equivalence) Control IC or F5111 IC diluted in 200 μL of PBS from day −3 to 0 prior to initiating anti-PD-1 treatment. Starting on day 0 (4 hours after the last IC treatment), mice were treated i.p. every 4 days with either PBS (control group) or 200 μg anti-PD-1 antibody (clone RMP1–14, Bio X Cell) for a total of four or five doses. Non-fasting blood glucose was monitored by using a OneTouch® Ultra® 2 glucometer. Diabetes onset was considered to have occurred when non-fasting blood glucose concentration exceeded 250 mg/dL for two consecutive measurements. Statistical significance was determined by pairwise comparisons using the Log-rank (Mantel-Cox) test.
VanDyke D., Iglesias M., Tomala J., Young A., Smith J., Perry J.A., Gebara E., Cross A.R., Cheung L.S., Dykema A.G., Orcutt-Jahns B.T., Henclová T., Golias J., Balolong J., Tomasovic L.M., Funda D., Meyer A.S., Pardoll D.M., Hester J., Issa F., Hunter C.A., Anderson M.S., Bluestone J.A., Raimondi G, & Spangler J.B. (2022). Engineered human cytokine/antibody fusion proteins expand regulatory T cells and confer autoimmune disease protection. Cell reports, 41(3), 111478.
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5

Co-stimulatory Blockade in Lung Transplant

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Left orthotopic vascularized lung transplants were performed as previously described (7 (link)). Mice were treated with co-stimulatory blockade consisting of MR1 (250 μg intraperitoneally) and CTLA4-Ig (200 μg intraperitoneally), on days 0 and 2, respectively (Bio X Cell, West Lebanon, NH). For select experiments, lung recipients were additionally treated with anti-PD-1 antibody (clone RMP1-14: 250 μg intraperitoneally, days −2, 2) (Bio X Cell, West Lebanon, NH). For some experiments, CD8+ T cells isolated from spleens of either B6 wildtype (CD45.2+Thy1.2+ or CD45.2+Thy1.1+) or PD-1-deficient (CD45.2+Thy1.2+) mice were injected into B6 CD45.1+Thy1.2+ recipients of BALB/c lungs at the time of transplantation.
Takahashi T., Hsiao H., Tanaka S., Li W., Higashikubo R., Scozzi D., Bharat A., Ritter J., Krupnick A., Gelman A, & Kreisel D. (2017). PD-1 expression on CD8+ T cells regulates their differentiation within lung allografts and is critical for tolerance induction. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 18(1), 216-225.
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6

Intracranial Tumor Immunotherapy with Reovirus and GM-CSF

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In vivo animal models were approved by the University of Leeds Local Ethics Review Committee or the Mayo Foundation Institutional Animal Care and Use Committee. For fig. S1, six- to 10-week old C57/BL6 mice (Jackson Laboratories) were injected intracranially with 1x105 B16 melanoma cells and eight days later treated with a single injection of 1x108 PFU i.v. reovirus or PBS. Mice were sacrificed three days after treatment. For Figure 5, eight mice in each group were used; six- to eight-week old C57/BL6 reovirus-vaccinated mice (22 (link)) were injected intracranially with GL261 cells on day one. On day five, mice were treated using daily i.v. injections of 300 ng GM-CSF (Peprotech) and i.v. reovirus at 5x107 PFU or PBS as a control for five days. Treatments were repeated for a further five consecutive days starting on day 12. On days 19, 21, and 23, mice were treated with anti-PD-1 antibody (clone RMP1-14; Bio X Cell) or IgG isotype control (clone MPC11; Bio X Cell) by i.p. injections. Mice were regularly monitored for any signs of deterioration or weight loss, upon which animals were sacrificed and the duration of survival recorded.
Samson A., Scott K.J., Taggart D., West E.J., Wilson E., Nuovo G.J., Thomson S., Corns R., Mathew R.K., Fuller M.J., Kottke T.J., Thompson J.M., Ilett E.J., Cockle J.V., van Hille P., Sivakumar G., Polson E.S., Turnbull S.J., Appleton E.S., Migneco G., Rose A.S., Coffey M.C., Beirne D.A., Collinson F.J., Ralph C., Anthoney D.A., Twelves C.J., Furness A.J., Quezada S.A., Wurdak H., Errington-Mais F., Pandha H., Harrington K.J., Selby P.J., Vile R.G., Griffin S.D., Stead L.F., Short S.C, & Melcher A.A. (2018). Intravenous Delivery of Oncolytic Reovirus to Brain Tumor Patients Immunologically Primes for Subsequent Checkpoint Blockade. Science translational medicine, 10(422), eaam7577.
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7

Murine Model of Malignant Pleural Disease

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Mice were anesthetized using inhaled isoflurane and oxygen delivery. Intrapleural inoculation with LLC at 5 × 105 cells in 120 μL of phosphate-buffered saline (PBS) was delivered percutaneously in the right hemithorax to establish the MPD model.18 (link),19 (link) After 1 intraperitoneal dose of D-luciferin (150 μg/mL), tumor burden was monitored by luciferase expression and light emission with a Xenogen IVIS 200 Optical In Vivo Imaging System (Caliper Life Sciences, Hopkinton, Mass). Seven days after tumor inoculation, mice were randomly assigned to various treatment groups: intrapleural PBS control, intrapleural virus (VV-YFP or VV-IL-2), systemic (intraperitoneal) VV-IL-2, or intrapleural viruses in combination with systemic (via peritoneum) anti–PD-1 antibody (clone RMP1–14; Bio X Cell; 200 μg per injection). Tumor burden was assessed by bioluminescent imaging as described next. Mice were killed when moribund. Seven days after treatment, bioluminescent imaging was completed and mice were euthanized to harvest spleen tissue and intrapleural tumor nodules (Figure 1, B). Of note, parenteral administration was done via the peritoneal route for all treatments.20 (link)
Ekeke C.N., Russell K.L., Murthy P., Guo Z.S., Soloff A.C., Weber D., Pan W., Lotze M.T, & Dhupar R. (2020). Intrapleural interleukin-2–expressing oncolytic virotherapy enhances acute antitumor effects and T-cell receptor diversity in malignant pleural disease. The Journal of thoracic and cardiovascular surgery, 163(4), e313-e328.
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8

Anti-PD-1 and Anti-CTLA-4 Immunotherapy in Mice

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MC38 tumor–bearing C57BL/6 mice were treated with an intraperitoneal injection of PBS (vehicle control) or 200 μg anti–PD-1 antibody (clone RMP1-14, BioXcell) on days 0, 3, and 6. LLC-bearing C57BL/6 mice were treated with PBS (vehicle control) or 200 μg anti–PD-1 plus 100 μg anti–CTLA-4 antibodies (clone 9D9, BioXcell) on days 0, 3, and 6. Mice were subjected to PET imaging at 0.5 hours following intravenous injection of 68Ga-grazytracer. Flow cytometric analysis of CD8, IFN-γ, and granzyme B was performed on day 9.
Zhou H., Wang Y., Xu H., Shen X., Zhang T., Zhou X., Zeng Y., Li K., Zhang L., Zhu H., Yang X., Li N., Yang Z, & Liu Z. (2022). Noninvasive interrogation of CD8+ T cell effector function for monitoring early tumor responses to immunotherapy. The Journal of Clinical Investigation, 132(16), e161065.
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9

Evaluating Anti-HER2 CAR-T Cell Efficacy

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Anti-HER2 CAR-T cells or in the presence of 20 μg/ml anti-PD1 antibody were incubated with HER2+ 4T1-Luc-HER2 cells at an effector: target ratio of 4:1 for 24 h in a 96-well plate. Anti-PD1 antibody (clone RMP1-14) was purchased from BioXCell (New Hampshire, USA). ELISA kits (R&D Systems, Inc. Minneapolis, USA) were used to analyze mouse IL-2 and IFN-γ concentrations in the supernatants of T cells according to the manufacturer's instructions. The co-cultures of HER2− 4T1 cells with anti-HER2 CAR-T cells (or in combination with anti-PD1 antibody), or HER2+ 4T1-Luc-HER2 cells with the blank T cells (or in combination with anti-PD1 antibody) were used as negative controls.
Li P., Yang L., Li T., Bin S., Sun B., Huang Y., Yang K., Shan D., Gu H, & Li H. (2020). The Third Generation Anti-HER2 Chimeric Antigen Receptor Mouse T Cells Alone or Together With Anti-PD1 Antibody Inhibits the Growth of Mouse Breast Tumor Cells Expressing HER2 in vitro and in Immune Competent Mice. Frontiers in Oncology, 10, 1143.
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10

Investigating Anti-PD-1 Response in Hepa1-6 Tumors

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Mice bearing orthotopic Hepa1-6 tumors were intraperitoneally injected with PBS or anti-PD-1 antibody (clone RMP1-14, BioXcell) on day 10, 14, 18, 22, and 26. On day 27, the whole tumors were collected and the surrounding tissue was removed. The tumors that had an intermediate response were excluded, and three largest tumors (the nonresponsive tumors) and three smallest tumors (the responsive tumors) compared with PBS-treated group were frozen in liquid nitrogen immediately. The RNA extraction, library preparation and sequencing were performed by Novogene (Beijing, China).
Zhang X., Wei Z., Yong T., Li S., Bie N., Li J., Li X., Liu H., Xu H., Yan Y., Zhang B., Chen X., Yang X, & Gan L. (2023). Cell microparticles loaded with tumor antigen and resiquimod reprogram tumor-associated macrophages and promote stem-like CD8+ T cells to boost anti-PD-1 therapy. Nature Communications, 14, 5653.
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