Anti-mouse PD-1 Antibody (CD279, RMP1-14.1) | PA007162.r2a
$150.00 – $700.00
Recombinant anti-mouse PD 1/ CD279 antibody(RMP1-14.1), which share the same variable region sequences with the rat anti-mouse PD-1 antibody (clone: RMP1-14), are produced from mammalian cells. Anti-mouse PD-1 / CD279 antibody (RMP1-14.1, rat IgG2a kappa) ‘s affintiy to the mouse PD-1 protein is <2 nM. The recombinant rat IgG2a isotype control available.
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| Catalog No. | PA007162.r2a |
|---|---|
| Product Name | Anti-mouse PD-1 Antibody (CD279, RMP1-14.1) | PA007162.r2a |
| Supplier Name | Syd Labs, Inc. |
| Brand Name | Syd Labs |
| Synonyms | Mouse Anti-Mouse PD 1 Monoclonal Antibodies, Murinized Anti-Mouse PD 1 Monoclonal Antibodies |
| Summary | The Anti-mouse PD-1 Antibody (RMP1-14.1, Rat IgG2a Kappa ) was produced in mammalian cells. |
| Clone | RMP1-14.1, the same variable region and constant region sequences as the rat anti-mouse PD-1 monoclonal antibody (clone number: RMP1-14) |
| Isotype | Rat IgG2a, kappa |
| Applications | immunohistochemistry (IHC), Flow Cytometry (FC), and various in vitro and in vivo functional assays. |
| Immunogen | The original rat hybridoma (clone name: RMP1-14) was generated by immunizing Sprague Dawley rats with mouse PD-1-transfected BHK cells and using a P3U1 myeloma as the fusion partner. |
| Form Of Antibody | 0.2 μM filtered solution of 1x PBS. |
| Endotoxin | Less than 1 EU/mg of protein as determined by LAL method. |
| Purity | >95% by SDS-PAGE under reducing conditions. |
| Shipping | The In Vivo Grade Recombinant Anti-mouse PD-1 Antibody (RMP1-14.1) are shipped with ice pack. Upon receipt, store it immediately at the temperature recommended below. |
| Stability & Storage | Use a manual defrost freezer and avoid repeated freeze-thaw cycles. 1 month from date of receipt, 2 to 8°C as supplied. 3 months from date of receipt, -20°C to -70°C as supplied. |
| Note | Recombinant mouse anti-mouse PD 1 / CD279 monoclonal antibodies, whose variable region sequences are murined from the rat anti-mouse PD-1 monoclonal antibody (clone number: RMP1-14), are produced from mammalian cells. The recombinant rat and chimeric mouse versions of the RMP1-14 antibody are also available. |
| Order Offline | Phone: 1-617-401-8149 Fax: 1-617-606-5022 Email: message@sydlabs.com Or leave a message with a formal purchase order (PO) Or credit card. |
Description
PA007162.r2a: Recombinant Anti-mouse PD-1 Antibody(Clone: CD279, RMP1-14.1), Rat IgG2a Kappa, In Vivo Grade
The anti mouse PD-1 antibody is widely recognized as a pivotal reagent in immunological studies, with the RMP1-14 antibody being a standout clone for targeting mouse PD-1 (CD279). This anti mouse pd 1 antibody is designed to interrupt the PD-1/PD-L1 pathway, a critical mechanism in immune checkpoint regulation, making it essential for research in cancer immunotherapy. Scientists often employ the anti mouse cd279 antibody in mouse models, such as those for lung cancer, to investigate how blocking PD-1 enhances T-cell activation and combats tumor growth. The RMP1-14 antibody also supports studies on immune tolerance in chronic infections and autoimmune conditions, offering insights into therapeutic development. Its precise binding to mouse PD-1 ensures reliable results, cementing its role as a cornerstone in advancing our understanding of immune responses.
Syd Labs provides anti-mouse PD1 monoclonal antibodies. The in vivo grade recombinant anti-mouse PD-1 monoclonal antibody (MAb Rat IgG2a Kappa) was produced in mammalian cells. Syd Labs presents a comprehensive array of anti-mouse PD 1 monoclonal antibody (mab) subtypes. These subtypes are crafted to meet different research needs and include Rat IgG2a Kappa, Rabbit IgG, and several Mouse IgG variants. Each of these antibody subtypes has distinct biochemical and functional characteristics, making them well – suited for various applications in immunology research.
References about Anti-mouse PD-1 (CD279, RMP1-14.1) MAb,please click: anti-mouse PD-1 monoclonal antibody (clone RMP1-14) referenced literature.
References for Anti-mouse PD-1 Antibody (RMP1-14):
1、Delivery of a BET protein degrader via a CEACAM6-targeted antibody-drug conjugate inhibits tumour growth in pancreatic cancer models.
Nakazawa, Y., et al. Nat Commun. 2024 Mar 11;15(1):2192. doi: 10.1038/s41467-024-46167-1. PMID: 38467634
“Anti-mouse PD-1 antibody was intraperitoneally injected on day 0 and day 7, and ADC was intravenously injected into the tail vein on day 0. …PDX tumors were extirpated from mice and digested with a Tumor Dissociation Kit and gentleMACS Dissociator (Miltenyi Biotec). …Seven days after drug administration, mice were sacrificed and tumors and draining lymph nodes were collected. …Pancreatic ductal adenocarcinoma (PDAC) has the worst prognosis of all cancers. …To improve PDAC therapy, we establish screening systems based on organoid and co-culture technologies and find a payload of antibody–drug conjugate (ADC), a bromodomain and extra-terminal (BET) protein degrader named EBET.”
2、Murine- and Human-Derived Autologous Organoid/Immune Cell Co-Cultures as Pre-Clinical Models of Pancreatic Ductal Adenocarcinoma.
Holokai, L., et al. Cancers (Basel). 2020 Dec 17;12(12):3816. doi: 10.3390/cancers12123816. PMID: 33348809
“Seven days post-transplantation, mice were treated with chemotherapeutics (gemcitabine plus paclitaxel-like Epothilone A), InVivoPlus anti-mouse PD-1 (CD279), cabozantinib (kinase inhibitor known to deplete MDSCs) or a combination of two or three of these drugs for a further 7 days post-orthotopic transplantation. …Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies, with an approximate 10% five-year survival rate despite therapy. …A plausible reason for this observation may be that other, redundant, immune-suppressive mechanisms are at play. …These studies present a pre-clinical organoid model that may be used to test the efficacy of combinatorial therapies and targeted therapies, based on modulating the tumor microenvironment, to improve cancer patient response and survival. …Myeloid-derived suppressor cells (MDSCs) are known to block anti-tumor CD8+ T cell immune responses in various cancers including pancreas.”
3、The Antitumor Activity of Combinations of Cytotoxic Chemotherapy and Immune Checkpoint Inhibitors Is Model-Dependent.
Grasselly, C., et al. Front Immunol. 2018 Oct 9;9:2100. doi: 10.3389/fimmu.2018.02100. PMID: 30356816
“As an example, monoclonal anti-PD-1 and anti-PD-L1 antibodies (mAb) showed impressive efficacy in clinical trials for the treatment of unresectable or metastatic melanoma, metastatic non-small cell lung cancer, renal cancer, and more recently for urothelial carcinoma and Hodgkin’s lymphoma. …For this reason, it is crucial to develop new therapeutic approaches to enhance the therapeutic effects of PD-1/PD-L1 blockade, and to avoid resistance phenomena. …We performed an exploratory study of various combination regimens of chemotherapies with immune checkpoint blockers anti-PD-1 and anti-PD-L1, in several murine syngeneic preclinical models. …In some cases however these maximally tolerated chemotherapy regimens did not significantly impact on the tumor growth of established tumors in some models (MC38, MB49, and MBT-2). …In the 4T1 breast cancer model, the combination of cyclophosphamide/doxorubicin with anti-PD-1 or anti-PD-L1 Mabs did not show any increased anti-tumor effect.”
4、Reversal of indoleamine 2,3-dioxygenase-mediated cancer immune suppression by systemic kynurenine depletion with a therapeutic enzyme.
Triplett, T. A., et al. Nat Biotechnol. 2018 Sep;36(8):758-764. doi: 10.1038/nbt.4180. PMID: 30010674
“Whether these effects are due to Trp depletion in the TME or mediated by the accumulation of the IDO1 and/or TDO (hereafter referred to as IDO1/TDO) product kynurenine (Kyn) remains controversial. …Here we show that administration of a pharmacologically optimized enzyme (PEGylated kynureninase; hereafter referred to as PEG-KYNase) that degrades Kyn into immunologically inert, nontoxic and readily cleared metabolites inhibits tumor growth. …Enzyme treatment was associated with a marked increase in the tumor infiltration and proliferation of polyfunctional CD8+ lymphocytes. …PEG-KYNase mediated prolonged depletion of Kyn in the TME and reversed the modulatory effects of IDO1/TDO upregulation in the TME. …Increased tryptophan (Trp) catabolism in the tumor microenvironment (TME) can mediate immune suppression by upregulation of interferon (IFN)-γ-inducible indoleamine 2,3-dioxygenase (IDO1) and/or ectopic expression of the predominantly liver-restricted enzyme tryptophan 2,3-dioxygenase (TDO).”
5、Eradication of large established tumors in mice by combination immunotherapy that engages innate and adaptive immune responses.
Moynihan, K. D., et al. Nat Med. 2016 Dec;22(12):1402-1410. doi: 10.1038/nm.4200. PMID: 27775706
“Checkpoint blockade with antibodies specific for cytotoxic T lymphocyte–associated protein (CTLA)-4 or programmed cell death 1 (PDCD1; also known as PD-1) elicits durable tumor regression in metastatic cancer, but these dramatic responses are confined to a minority of patients. …This suboptimal outcome is probably due in part to the complex network of immunosuppressive pathways present in advanced tumors, which are unlikely to be overcome by intervention at a single signaling checkpoint. …Here we describe a combination immunotherapy that recruits a variety of innate and adaptive immune cells to eliminate large tumor burdens in syngeneic tumor models and a genetically engineered mouse model of melanoma; to our knowledge tumors of this size have not previously been curable by treatments relying on endogenous immunity. …Maximal antitumor efficacy required four components: a tumor-antigen-targeting antibody, a recombinant interleukin-2 with an extended half-life, anti-PD-1 and a powerful T cell vaccine. …Depletion experiments revealed that CD8+ T cells, cross-presenting dendritic cells and several other innate immune cell subsets were required for tumor regression.”
6、TGFβ Is a Master Regulator of Radiation Therapy-Induced Antitumor Immunity.
Vanpouille-Box, C., et al. Cancer Res. 2015 Jun 1;75(11):2232-42. doi: 10.1158/0008-5472.CAN-14-3511. PMID: 25858148
“1D11, a pan-isoform, TGFβ-neutralizing mouse mAb that binds only to active TGFβ (26) or 13C4 isotype mAb was provided by Genzyme Inc. Anti–PD-1 RMP1-14 mAb was purchased from BioXCell. …T cells directed to endogenous tumor antigens are powerful mediators of tumor regression. …Eliciting T-cell responses to a patient’s individual tumor remains a major challenge. …We hypothesized that TGFβ activity is a major obstacle hindering the ability of radiation to generate an in situ tumor vaccine. …Gene signatures associated with IFNγ and immune-mediated rejection were detected in tumors treated with radiation therapy and TGFβ blockade in combination but not as single agents.”
7、Radiation and dual checkpoint blockade activate non-redundant immune mechanisms in cancer.
Twyman-Saint Victor, C., et al. Nature. 2015 Apr 16;520(7547):373-7. doi: 10.1038/nature14292. PMID: 25754329
“This raises fundamental questions about mechanisms of non-redundancy and resistance. …Here we report major tumour regressions in a subset of patients with metastatic melanoma treated with an anti-CTLA4 antibody (anti-CTLA4) and radiation, and reproduced this effect in mouse models. …Unbiased analyses of mice revealed that resistance was due to upregulation of PD-L1 on melanoma cells and associated with T-cell exhaustion. …Radiation enhances the diversity of the T-cell receptor (TCR) repertoire of intratumoral T cells. …Similarly to results from mice, patients on our clinical trial with melanoma showing high PD-L1 did not respond to radiation plus anti-CTLA4, demonstrated persistent T-cell exhaustion, and rapidly progressed.”
8、PD-1 Co-inhibitory and OX40 Co-stimulatory Crosstalk Regulates Helper T Cell Differentiation and Anti-Plasmodium Humoral Immunity.
Zander, R. A., et al. Cell Host Microbe. 2015 May 13;17(5):628-41. doi: 10.1016/j.chom.2015.03.007. PMID: 25891357
“Human and mouse cells were analyzed with flow cytometry as detailed in the Supplemental Experimental Procedures. …The differentiation and protective capacity of Plasmodium-specific T cells are regulated by both positive and negative signals during malaria, but the molecular and cellular details remain poorly defined. …Here we show that malaria patients and Plasmodium-infected rodents exhibit atypical expression of the co-stimulatory receptor OX40 on CD4 T cells and that therapeutic enhancement of OX40 signaling enhances helper CD4 T cell activity, humoral immunity, and parasite clearance in rodents. …However, these beneficial effects of OX40 signaling are abrogated following coordinate blockade of PD-1 co-inhibitory pathways, which are also upregulated during malaria and associated with elevated parasitemia. …Our results show that targeting OX40 can enhance Plasmodium control and that crosstalk between co-inhibitory and co-stimulatory pathways in pathogen-specific CD4 T cells can impact pathogen clearance.”
9、Antibody Blockade of Semaphorin 4D Promotes Immune Infiltration into Tumor and Enhances Response to Other Immunomodulatory Therapies.
Evans, E. E., et al. Cancer Immunol Res. 2015 Jun;3(6):689-701. doi: 10.1158/2326-6066.CIR-14-0171. PMID: 25614511
“All mouse experiments were carried out according to the guidelines of the NIH and the University Committee on Animal Resources (UCAR) at the University of Rochester (Rochester, NY) for the care and use of laboratory animals. …Fifty microliters of supernatant was analyzed using BD’s mouse Inflammation CBA kit on a FACSCanto II flow cytometer. …Semaphorin 4D (SEMA4D, CD100) and its receptor plexin-B1 (PLXNB1) are broadly expressed in murine and human tumors, and their expression has been shown to correlate with invasive disease in several human tumors. …We describe a novel immunomodulatory function of SEMA4D, whereby strong expression of SEMA4D at the invasive margins of actively growing tumors influences the infiltration and distribution of leukocytes in the TME. …The immunomodulatory activity of anti-SEMA4D antibody can be enhanced by combination with other immunotherapies, including immune checkpoint inhibition and chemotherapy.”
10、A Threshold Level of Intratumor CD8+ T-cell PD1 Expression Dictates Therapeutic Response to Anti-PD1.
Ngiow, S. F., et al. Cancer Res. 2015 Sep 15;75(18):3800-11. doi: 10.1158/0008-5472.CAN-15-1082. PMID: 26208901
“Purified anti-mouse PD1 mAb (RMP1-14), anti-mouse Tim3 (RMT3-23), anti-mouse PDL1 (10F.9G2), and control Ig (2A3) were purchased from BioXCell and used in the schedule and dose as indicated. …We set out to compare the intratumor effects of anti-mouse PD1 therapy in sensitive and resistant mouse tumors where CD8+ T cells were prominent. …To assess the role of Treg in modulating intratumor T-cell PD1, we used a Foxp3-DTR transgenic mouse model to conditionally deplete Treg in both the MC38 and AT3 tumor models. …While this is a significant step forward, a greater interrogation of both mouse models and patient-derived material may lead to an even more sophisticated understanding. …We use mouse tumor models of anti-PD1 sensitivity and resistance and flow cytometry to assess tumor-infiltrating immune cells immediately after therapy.”
Related Recombinant IgG Reference Antibodies:
Recombinant Mouse IgG1 Isotype Control Antibody and Mutants, In vivo Grade
Recombinant Mouse IgG2a Isotype Control Antibody and Mutants, In vivo Grade
Recombinant Mouse IgG2c Isotype Control Antibody and Mutants, In vivo Grade
Recombinant Rat IgG2a Isotype Control Antibody, In vivo Grade
Syd Labs provides the following anti-mouse PD-L1 / PD-1 antibodies:
Recombinant anti-mouse PD1 antibodies (Clone 29F.1A12.1), In vivo grade
Recombinant anti-mouse PD-1 antibodies (Clone RMP1-14.1), In vivo grade
Recombinant anti-mouse PD-L1 antibodies (Clone 10F.9G2.1), In vivo grade
Recombinant anti-mouse PD-1 / PD-1 bispecific antibodies (Clone RMP1-14.1 / 29F.1A12.1), In vivo grade
Recombinant anti-mouse PD-1 / PD-1 bispecific antibodies (Clone 29F.1A12.1 / RMP1-14.1), In vivo grade
Recombinant anti-mouse PD-1 / PD-L1 bispecific antibodies (Clone RMP1-14.1 / 10F.9G2.1), In vivo grade
Recombinant anti-mouse PD-L1 / PD-1 bispecific antibodies (Clone 10F.9G2.1 / RMP1-14.1), In vivo grade
Recombinant anti-mouse PD-1 / PD-L1 bispecific antibodies (Clone 29F.1A12.1 / 10F.9G2.1), In vivo grade
Recombinant anti-mouse PD-L1 / PD-1 bispecific antibodies (Clone 10F.9G2.1 / 29F.1A12.1), In vivo grade
Questions and Answers about recombinant anti-mouse PD-1 (CD279, Clone RMP1-14) antibody:
Question: Which anti-mouse PD1 antibody works the best?
Answer: (by AI) There are several anti-mouse PD1 antibodies available in the market: Clones RMP1-14, 29F.1A12, and J43. All three of these antibodies are commonly used to block PD-1 signaling in vivo in murine tumor models and other mouse models. These three clones all have extensive multi-year publication records supporting them. The RMP1-14 antibody has been reported to block the binding of PD-1 to its ligands (B7-H1 and B7-DC) and to inhibit T cell proliferation and cytokine production costimulated by macrophages (but not by dendritic cells and B cells). (by Syd Labs) Syd Labs offers anti-mouse PD-1 monoclonal antibodies based on the sequences of clones RMP1-14 and 29F.1A12. Syd Labs provides in vivo grade recombinant antibodies including engineered antibodies for the clones RMP1-14 and 29F.1A12. Even though mouse and rat are close, rat antibodies may still induce immunogenecity in mice. Antibodies with murinized variable regions and mouse constant regions behave like humanized antibody drugs in animal models using mice. In addition, the mouse IgG2c antibody is produced in certain inbred strains such as C57BL/6, C57BL/10, SJL, and NOD, which does not express the mouse IgG2a antibody; the mouse IgG2a antibody is produced in other inbred strains such as BALB/c and Swiss Webster mice, which does not express the mouse IgG2c antibody. If one uses the C57BL/6 mouse strain for animal model research, it is better to use the IgG2c antibodies rather than the IgG2a antibodies. The format with the Fc silenced, Fc silent, or Fcs with silenced effector function, such as LALAPG mutation, is the most popular for anti-mouse PD1 antibodies (clones RMP1-14 and 29F.1A12) and anti-mouse PD-L1 antibodies (clone 10F.9G2).
Question: Do you produce any recombinant Fc-silenced RMP1-14 antibody?
Answer: Sure, we provide various recombinant Fc silent RMP1-14 antibodies, such as mIgG2c LALAPG, mIgG2a LALAPG, and mIgG1 D265A. We also provide custom recombinant antibody production service to produce other engineered versions of recombinant RMP1-14 antibodies. We have a promotion program running: We provide 1 mg PA007162.m2cLA (In Vivo Grade Recombinant Anti-mouse PD-1 Mouse IgG2c-LALAPG Kappa Monoclonal Antibody (Clone RMP1-14.1)) for free in exchange of results. Please contact us to know more about the free RMP1-14 antibody.
Question: What is the difference among PA007162.r2a, PA007162.m2cLA, and PA007162.mm2cLA?
Answer: PA007162.r2a is the recombinant anti-mouse PD-1 monoclonal antibody (rat IgG2a kappa, clone RMP1-14.1) produced in CHO cells or HEK293 cells if needed. It has the same variable region and constant region sequences as the rat anti-mouse PD-1 monoclonal antibody from the hybridoma clone of RMP1-14. Rat antibodies may cause high immuogenicity in mice; thus, at least recombinant antibodies with mouse antibody constant regions should be used to replace the rat antibody constant regions. PA007162.m2cLA is the recombinant anti-mouse PD-1 antibody (clone RMP1-14.1) whose constant regions are mouse IgG2c LALAPG kappa. We further murinize the antibody variable region sequences of PA007162.m2cLA to produce PA007162.mm2cLA.
anti-mouse PD-1 Antibody (CD279, RMP1-14.1) from: Anti-Mouse PD1 Monoclonal Antibodies: PA007162.r2a Syd Labs

