Anti-mouse PD-1 Antibody (RMP1-14.1, Mouse IgG2a) | PA007162.m2a

Catalog No.	PA007162.m2a
Product Name	Anti-mouse PD-1 Antibody (RMP1-14.1, Mouse IgG2a) | PA007162.m2a
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 In Vivo Grade Recombinant Anti-mouse PD-1 Mouse IgG2a Kappa Monoclonal Antibody (Clone RMP1-14.1) was produced in mammalian cells.
Clone	RMP1-14.1, the same variable region sequences as the rat anti-mouse PD-1 monoclonal antibody (clone number: RMP1-14)
Isotype	mouse 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 rats with mouse PD-1-transfected BHK cells.
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 Mouse IgG2a Kappa Monoclonal Antibody (Clone 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.m2a: Anti-mouse PD-1 Monoclonal Antibody (RMP1-14.1), Mouse IgG2a Kappa, In Vivo Grade Recombinant
The in vivo grade recombinant murinized rat anti-mouse PD-1 monoclonal antibody (mouse IgG2c-LALAPG kappa) was produced in mammalian cells.

References for anti-mouse PD-1 antibody(RMP1-14):

1、The critical role of CD4+ T cells in PD-1 blockade against MHC-II–expressing tumors such as classic Hodgkin lymphoma
Joji Nagasaki,et al.Blood Adv. 2020.PMCID: PMC7479950
“Classic Hodgkin lymphoma (cHL) responds markedly to PD-1 blockade therapy, and the clinical responses are reportedly dependent on expression of major histocompatibility complex class II (MHC-II). This dependence is different from other solid tumors, in which the MHC class I (MHC-I)/CD8+ T-cell axis plays a critical role. In this study, we investigated the role of the MHC-II/CD4+ T-cell axis in the antitumor effect of PD-1 blockade on cHL. In cHL, MHC-I expression was frequently lost, but MHC-II expression was maintained. CD4+ T cells highly infiltrated the tumor microenvironment of MHC-II–expressing cHL, regardless of MHC-I expression status. Consequently, CD4+ T-cell, but not CD8+ T-cell, infiltration was a good prognostic factor in cHL, and PD-1 blockade showed antitumor efficacy against MHC-II–expressing cHL associated with CD4+ T-cell infiltration. Murine lymphoma and solid tumor models revealed the critical role of antitumor effects mediated by CD4+ T cells: an anti-PD-1 monoclonal antibody exerted antitumor effects on MHC-I−MHC-II+ tumors but not on MHC-I−MHC-II− tumors, in a cytotoxic CD4+ T-cell–dependent manner. Furthermore, LAG-3, which reportedly binds to MHC-II, was highly expressed by tumor-infiltrating CD4+ T cells in MHC-II–expressing tumors. Therefore, the combination of LAG-3 blockade with PD-1 blockade showed a far stronger antitumor immunity compared with either treatment alone. We propose that PD-1 blockade therapies have antitumor effects on MHC-II–expressing tumors such as cHL that are mediated by cytotoxic CD4+ T cells and that LAG-3 could be a candidate for combination therapy with PD-1 blockade.”

2、Contribution of NK cells to immunotherapy mediated by PD-1/PD-L1 blockade
Joy Hsu,et al.J Clin Invest. 2018.PMCID: PMC6159991
“Checkpoint blockade immunotherapy targeting the PD-1/PD-L1 inhibitory axis has produced remarkable results in the treatment of several types of cancer. Whereas cytotoxic T cells are known to provide important antitumor effects during checkpoint blockade, certain cancers with low MHC expression are responsive to therapy, suggesting that other immune cell types may also play a role. Here, we employed several mouse models of cancer to investigate the effect of PD-1/PD-L1 blockade on NK cells, a population of cytotoxic innate lymphocytes that also mediate antitumor immunity. We discovered that PD-1 and PD-L1 blockade elicited a strong NK cell response that was indispensable for the full therapeutic effect of immunotherapy. PD-1 was expressed on NK cells within transplantable, spontaneous, and genetically induced mouse tumor models, and PD-L1 expression in cancer cells resulted in reduced NK cell responses and generation of more aggressive tumors in vivo. PD-1 expression was more abundant on NK cells with an activated and more responsive phenotype and did not mark NK cells with an exhausted phenotype. These results demonstrate the importance of the PD-1/PD-L1 axis in inhibiting NK cell responses in vivo and reveal that NK cells, in addition to T cells, mediate the effect of PD-1/PD-L1 blockade immunotherapy.”

3、Sources of inter-individual variability leading to significant changes in anti-PD-1 and anti-PD-L1 efficacy identified in mouse tumor models using a QSP framework
Jessica C Leete,et al.Front Pharmacol. 2022.PMCID: PMC9760747
“While anti-PD-1 and anti-PD-L1 [anti-PD-(L)1] monotherapies are effective treatments for many types of cancer, high variability in patient responses is observed in clinical trials. Understanding the sources of response variability can help prospectively identify potential responsive patient populations. Preclinical data may offer insights to this point and, in combination with modeling, may be predictive of sources of variability and their impact on efficacy. Herein, a quantitative systems pharmacology (QSP) model of anti-PD-(L)1 was developed to account for the known pharmacokinetic properties of anti-PD-(L)1 antibodies, their impact on CD8+ T cell activation and influx into the tumor microenvironment, and subsequent anti-tumor effects in CT26 tumor syngeneic mouse model. The QSP model was sufficient to describe the variability inherent in the anti-tumor responses post anti-PD-(L)1 treatments. Local sensitivity analysis identified tumor cell proliferation rate, PD-1 expression on CD8+ T cells, PD-L1 expression on tumor cells, and the binding affinity of PD-1:PD-L1 as strong influencers of tumor growth. It also suggested that treatment-mediated tumor growth inhibition is sensitive to T cell properties including the CD8+ T cell proliferation half-life, CD8+ T cell half-life, cytotoxic T-lymphocyte (CTL)-mediated tumor cell killing rate, and maximum rate of CD8+ T cell influx into the tumor microenvironment. Each of these parameters alone could not predict anti-PD-(L)1 treatment response but they could shift an individual mouse’s treatment response when perturbed. The presented preclinical QSP modeling framework provides a path to incorporate potential sources of response variability in human translation modeling of anti-PD-(L)1.”

4、4-1BB Agonism Averts TIL Exhaustion and Licenses PD-1 Blockade in Glioblastoma and Other Intracranial Cancers
Karolina I Woroniecka,et al.Clin Cancer Res. 2020.PMCID: PMC7073290
“Purpose:
The success of checkpoint blockade against glioblastoma (GBM) has been disappointing. Anti-PD-1 strategies may be hampered by severe T-cell exhaustion. We sought to develop a strategy that might license new efficacy for checkpoint blockade in GBM.
Experimental Design:
We characterized 4-1BB expression in tumor infiltrating lymphocytes (TIL) from human GBM. We implanted murine tumor models including glioma (CT2A), melanoma (B16), breast (E0771), and lung carcinomas (LLC) intracranially (IC) and subcutaneously (SC), characterized 4-1BB expression, and tested checkpoint blockade strategies in vivo.
Results:
Our data reveal that 4-1BB is frequently present on non-exhausted CD8+ tumor-infiltrating lymphocytes (TIL) in human and murine GBM. In murine gliomas, 4-1BB agonism and PD-1 blockade demonstrate a synergistic survival benefit in a CD8+ T-cell dependent manner. The combination decreases TIL exhaustion and improves TIL functionality. This strategy proves most successful against intracranial (IC) CT2A gliomas. Efficacy in all instances correlates with the levels of 4-1BB expression on CD8+ TIL, rather than with histology or with IC versus SC tumor location. Proffering 4-1BB expression to T-cells licenses combination 4-1BB agonism and PD-1 blockade in models where TIL 4-1BB levels had previously been low and the treatment ineffective.”

5、The Programmed Death-1 Pathway Counter-Regulates Inflammation-Induced Osteoclast Activity in Clinical and Experimental Settings
Stinne R Greisen,et al.Front Immunol. 2022.PMCID: PMC8959817
“Objective
The programmed death-1 (PD-1) pathway is essential for maintaining self-tolerance and plays an important role in autoimmunity, including rheumatoid arthritis (RA). Here, we investigated how membrane-bound and soluble (s)PD-1 influence bone homeostasis during chronic inflammation, exemplified in RA.
Methods
Bone mineral density and bone microstructure were examined in PD-1 and PD-L1 knockout (KO) mice and compared with wild-type (WT) mice. Receptor activator of nuclear factor kappa-B ligand (RANKL) was measured in serum, and the expression examined on activated bone marrow cells. Osteoclast formation was examined in cells from murine spleen and bone marrow and from human synovial fluid cells. sPD-1 was measured in chronic and early (e)RA patients and correlated to markers of disease activity and radiographic scores.
Results
PD-1 and PD-L1 KO mice showed signs of osteoporosis. This was supported by a significantly reduced trabecular bone volume fraction and deteriorated microstructure, as well as increased osteoclast formation and an increased RANKL/OPG ratio. The recombinant form of sPD-1 decreased osteoclast formation in vitro, but was closely associated with disease activity markers in eRA patients. Sustained elevated sPD-1 levels indicated ongoing inflammation and were associated with increased radiographic progression.”

6、Dying cells expose a nuclear antigen cross-reacting with anti-PD-1 monoclonal antibodies
Philipp Metzger,et al.Sci Rep. 2018.PMCID: PMC5995819
“Checkpoint molecules such as programmed death 1 (PD-1) dampen excessive T cell activation to preserve immune homeostasis. PD-1-specific monoclonal antibodies have revolutionized cancer therapy, as they reverse tumour-induced T cell exhaustion and restore CTL activity. Based on this success, deciphering underlying mechanisms of PD-1-mediated immune functions has become an important field of immunological research. Initially described for T cells, there is emerging evidence of unconventional PD-1 expression by myeloid as well as tumor cells, yet, with cell-intrinsic functions in various animal tumor models. Here, we describe positive PD-1 antibody staining of various murine immune and tumour cells that is, unlike for T cells, not the PD-1 receptor and restricted to cells with low forward scatter characteristics. Based on flow cytometry and various approaches, including two established murine anti-PD-1 antibody clones, CRISPR/Cas9 genome editing and confocal imaging, we describe a staining pattern assigned to a nuclear antigen cross-reacting with anti-PD-1 monoclonal antibodies. Lack of PD-1 expression was further underlined by the analysis of PD-1 expression from B16-F10-derived 3D cultures and ex vivo tumours. Thus, our data provide multiple lines of evidence that PD-1 expression by non-T cells is unlikely to be the case and, taking recent data of PD-1 tumour cell-intrinsic functions into account, suggest that other antibody-mediated pathways might apply.”

7、Targeting PD-L2/RGMb overcomes microbiome-related immunotherapy resistance
Joon Seok Park,et al.Nature. 2023.PMCID: PMC10219577
“The gut microbiota has been shown to be a critical regulator of anti-tumor immunity during immune checkpoint inhibitor therapies. Several bacteria that promote an anti-tumor response to immune checkpoint inhibitors have been identified in mice(1-6), and transplantation of fecal specimens from responders has been shown to improve the efficacy of anti-PD-1 therapy in melanoma patients(7, 8). However, the increased efficacy from fecal transplants is variable and how gut bacteria promote anti-tumor immunity remains unclear. Here, we show that the gut microbiome downregulates expression of PD-L2 and its binding partner Repulsive Guidance Molecule b (RGMb) to promote anti-tumor immunity and identify bacterial species that mediate this effect. PD-L1 and PD-L2 share PD-1 as a binding partner, but PD-L2 can also bind RGMb. We demonstrate that blockade of PD-L2/RGMb interactions can overcome microbiome-dependent resistance to PD-1 pathway inhibitors: antibody-mediated blockade of the PD-L2/RGMb pathway or conditional deletion of RGMb in T cells combined with anti-PD-1 or anti-PD-L1 promotes anti-tumor responses in multiple mouse tumor models that do not respond to anti-PD-1 or anti-PD-L1 alone (Germ Free mice, antibiotic treated mice, and even mice colonized with non-responder patient stool). These studies identify downregulation of the PD-L2/RGMB pathway as a specific mechanism by which the gut microbiota can promote responses to PD-1 checkpoint blockade and define a potentially effective immunological strategy for treating patients who do not respond to PD-1 cancer immunotherapy.”

8、Host immunity following near-infrared photoimmunotherapy is enhanced with PD-1 checkpoint blockade to eradicate established antigenic tumors
Tadanobu Nagaya,et al.Cancer Immunol Res. 2021.PMCID: PMC8237708
“Near-infrared photoimmunotherapy (NIR-PIT) induces immunogenic cell death, but has mostly failed to induce durable antitumor responses in syngenic tumor mouse models. We hypothesized that adaptive immune resistance could be limiting durable responses after treatmemt with NIR-PIT. We investigated the effects of combining NIR-PIT targeting cell surface CD44 and PD-1 blockade in multiple syngeneic tumor models. In two of three models, NIR-PIT monotherapy halted tumor growth, enhanced dendritic cell tumor infiltration, and induced de novo tumor antigen-specific T-cell responses absent at baseline. The addition of PD-1 blockade reversed adaptive immune resistance, resulting in both enhanced pre-existing tumor antigen-specific T-cell responses and enhanced de novo T-cell responses induced by NIR-PIT. Enhanced immune responses correlated with shared tumor antigen expression, suggesting that antigenicity is a major determinant of response to combination NIR-PIT and PD-1 blockade. Combination treatment induced complete rejection of MC38 tumors treated with NIR-PIT, as well as untreated, distant tumors. Accordingly, tumor antigen-specific T-cell responses were measured in both treated and untreated tumors, validating the development of systemic antitumor immunity. Mice that cleared tumors resisted subsequent tumor challenge, indicating the presence of systemic immune memory. Cumulatively these results demonstrate reversal of adaptive immune resistance following induction of innate and adaptive immunity by NIR-PIT, resulting in high rates of tumor rejection and/or significant tumor growth control in antigenic syngeneic models of cancer.”

9、Cardiac myosin-specific autoimmune T cells contribute to immune-checkpoint-inhibitor-associated myocarditis
Taejoon Won,et al.Cell Rep. 2024.PMCID: PMC11108585
“Immune checkpoint inhibitors (ICIs) are an effective therapy for various cancers; however, they can induce immune-related adverse events (irAEs) as a side effect. Myocarditis is an uncommon, but fatal, irAE caused after ICI treatments. Currently, the mechanism of ICI-associated myocarditis is unclear. Here, we show the development of myocarditis in A/J mice induced by anti-PD-1 monoclonal antibody (mAb) administration alone without tumor cell inoculation, immunization, or viral infection. Mice with myocarditis have increased cardiac infiltration, elevated cardiac troponin levels, and arrhythmia. Anti-PD-1 mAb treatment also causes irAEs in other organs. Autoimmune T cells recognizing cardiac myosin are activated and increased in mice with myocarditis. Notably, cardiac myosin-specific T cells are present in naive mice, showing a phenotype of antigen-experienced T cells. Collectively, we establish a clinically relevant mouse model for ICI-associated myocarditis and find a contribution of cardiac myosin-specific T cells to ICI-associated myocarditis development and pathogenesis.”

10、Enhancing anti-tumor efficacy and immune memory by combining 3p-GPC-3 siRNA treatment with PD-1 blockade in hepatocellular carcinoma
Liwei Shao,et al.Oncoimmunology. 2022.PMCID: PMC9746623
“Hepatocellular carcinoma (HCC) is associated with a high mortality rate and presents a major challenge for human health. Activation of multiple oncogenes has been reported to be strongly associated with the progression of HCC. Moreover, the immunosuppressive tumor microenvironment (TME) and the host immune system are also implicated in the development of malignant HCC tumors. Glypican-3 (GPC-3), a proteoglycan involved in the regulation of cell proliferation and apoptosis, is aberrantly expressed in HCC. We synthesized a short 5ʹ-triphosphate (3p) RNA targeting GPC-3, 3p-GPC-3 siRNA, and found that it effectively inhibited subcutaneous HCC growth by raising type I IFN levels in tumor cells and serum and promoting tumor cell apoptosis. Moreover, 3p-GPC-3 siRNA was able to enhance the activation of CD4+ T cells, CD8+ T cells, and natural killer (NK) cells while reducing the proportion of regulatory T cells (Tregs) in the TME. Most intriguingly, a blocking anti-PD-1 antibody improved the anti-tumor effect of 3p-GPC-3 siRNA, predominantly by activating the immune response, reversing immune exhaustion, and improving immune memory. Our study suggests that the combination of 3p-GPC-3 siRNA administration and PD-1 blockade may represent a promising therapeutic strategy for HCC.”

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 monoclonal antibodies (Clone 29F.1A12.1), In vivo Grade
recombinant anti-mouse PD-1 monoclonal antibodies (Clone RMP1-14.1), In vivo Grade
recombinant anti-mouse PD-L1 monoclonal antibodies (Clone 10F.9G2.1), In vivo Grade

Anti-mouse PD-1 Monoclonal Antibody (RMP1-14.1) from: In Vivo Grade Recombinant Anti-mouse PD-1 Mouse IgG2a Kappa Monoclonal Antibody (Clone RMP1-14.1): PA007162.m2a Syd Labs

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