Anti-mouse PD-1 Monoclonal Antibody (RMP1-14.1) | PA007162.m2cLA

Catalog No.	PA007162.m2cLA
Product Name	Anti-mouse PD-1 Monoclonal Antibody (RMP1-14.1) | PA007162.m2cLA
Supplier Name	Syd Labs, Inc.
Brand Name	Syd Labs
Synonyms	Programmed Cell Death Protein 1, PD-1, CD279, Cluster of Differentiation 279, RMP1-14
Summary	Recombinant Anti-mouse PD-1 Monoclonal Antibody (Clone RMP1-14.1) , Mouse IgG2c-LALAPG Kappa 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 IgG2c, kappa.
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	Anti-mouse PD-1 Monoclonal Antibody (Clone RMP1-14.1) , Mouse IgG2c-L234A L235A P329G (LALAPG) Kappa 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 anti-mouse PD 1 / CD279 monoclonal antibodies, which share the same variable region sequences with the rat anti-mouse PD-1 antibody (clone number: RMP1-14), are produced from mammalian cells. The recombinant mouse anti-mouse PD 1 version of the RMP1-14 antibody is 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.m2cLA: Anti-mouse PD-1 Monoclonal Antibody (RMP1-14.1), Mouse IgG2c-L234A L235A P329G (LALAPG) Kappa, In Vivo Grade Recombinant

Syd Labs’s in vivo grade recombinant rat anti-mouse PD-1 monoclonal antibody (mouse IgG2c-LALAPG kappa) was produced in mammalian cells. Its affintiy to the mouse PD-1 protein is <2 nM. Recombinant anti-mouse PD-1/CD279 monoclonal antibody shares identical variable region sequences with the rat anti-mouse PD-1 antibody (Clone: RMP1-14). The constant region of Syd Labs’ Anti-mouse PD-1 Mouse IgG2c-LALAPG Kappa Monoclonal Antibody (Clone RMP1-14.1) is mouse IgG2c-LALAPG Kappa, which can be used in conjunction with the recombinant mouse IgG2c-LALAPG isotype control antibody. Sample preparation conditions and optimal dilution factors should be determined by researchers through experimental optimization.

Anti-mouse PD-1 Mouse IgG2c-L234A L235A P329G (LALAPG) Kappa Monoclonal Antibody (Clone RMP1-14.1) （PA007162.m2cLA Syd Labs）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 Recombinant Murinized Anti-mouse PD-1 Mouse IgG2c-L234A L235A P329G (LALAPG) Kappa Monoclonal Antibody (Clone RMP1-14.1) （PA007162.mm2cLA Syd Labs）.

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

1、PD-L1/PD-1 checkpoint pathway regulates hippocampal neuronal excitability and learning and memory behavior
Junli Zhao,et al.Neuron. 2024.PMCID: PMC10529885
“Programmed death protein 1 (PD-1) and its ligand PD-L1 constitute an immune checkpoint pathway. We report that neuronal PD-1 signaling regulates learning/memory in health and disease. Mice lacking PD-1 (encoded by Pdcd1) exhibit enhanced long-term potentiation (LTP) and memory. Intraventricular administration of anti-mouse PD-1 monoclonal antibody (RMP1-14) potentiated learning and memory. Selective deletion of PD-1 in excitatory neurons (but not microglia) also enhanced LTP and memory. Traumatic brain injury (TBI) impairs learning and memory, which is rescued by Pdcd1 deletion or intraventricular PD-1 blockade. Conversely, re-expression of Pdcd1 in PD-1 deficient hippocampal neurons suppresses memory and LTP. Exogenous PD-L1 suppressed learning/memory in mice and the excitability of mouse and NHP hippocampal neurons through PD-1. Notably, neuronal activation suppressed PD-L1 secretion, and PD-L1/PD-1 signaling is distinctly regulated by learning and TBI. Thus, conditions that reduce PD-L1 levels or PD-1 signaling could promote memory in both physiological and pathological conditions.”

2、Diphtheria toxin‐derived, anti‐PD‐1 immunotoxin, a potent and practical tool to selectively deplete PD‐1+ cells
Tianxiao Zhang,et al.Protein Sci. 2023.PMCID: PMC10443333
“Programmed death‐1 (PD‐1), an immune checkpoint receptor, is expressed on activated lymphocytes, macrophages, and some types of tumor cells. While PD‐1+ cells have been implicated in outcomes of cancer immunity, autoimmunity, and chronic infections, the exact roles of these cells in various physiological and pathological processes remain elusive. Molecules that target and deplete PD‐1+ cells would be instrumental in defining the roles unambiguously. Previously, an immunotoxin has been generated for the depletion of PD‐1+ cells though its usage is impeded by its low production yield. Thus, a more practical molecular tool is desired to deplete PD‐1+ cells and to examine functions of these cells. We designed and generated a novel anti‐PD1 diphtheria immunotoxin, termed PD‐1 DIT, targeting PD‐1+ cells. PD‐1 DIT is comprised of two single chain variable fragments (scFv) derived from an anti‐PD‐1 antibody, coupled with the catalytic and translocation domains of the diphtheria toxin. PD‐1 DIT was produced using a yeast expression system that has been engineered to efficiently produce protein toxins. The yield of PD‐1 DIT reached 1–2 mg/L culture, which is 10 times higher than the previously reported immunotoxin. Flow cytometry and confocal microscopy analyses confirmed that PD‐1 DIT specifically binds to and enters PD‐1+ cells. The binding avidities between PD‐1 DIT and two PD‐1+ cell lines are approximately 25 nM. Moreover, PD‐1 DIT demonstrated potent cytotoxicity toward PD‐1+ cells, with a half maximal effective concentration (EC50) value of 1 nM. In vivo experiments further showed that PD‐1 DIT effectively depleted PD‐1+ cells and enabled mice inoculated with PD‐1+ tumor cells to survive throughout the study. Our findings using PD‐1 DIT revealed the critical role of pancreatic PD‐1+ T cells in the development of type‐1 diabetes (T1D). Additionally, we observed that PD‐1 DIT treatment ameliorated relapsing–remitting experimental autoimmune encephalomyelitis (RR‐EAE), a mouse model of relapsing–remitting multiple sclerosis (RR‐MS). Lastly, we did not observe significant hepatotoxicity in mice treated with PD‐1 DIT, which had been reported for other immunotoxins derived from the diphtheria toxin. With its remarkable selective and potent cytotoxicity toward PD‐1+ cells, coupled with its high production yield, PD‐1 DIT emerges as a powerful biotechnological tool for elucidating the physiological roles of PD‐1+ cells. Furthermore, the potential of PD‐1 DIT to be developed into a novel therapeutic agent becomes evident.”

3、PD-L1 signaling selectively regulates T cell lymphatic transendothelial migration
Wenji Piao,et al.Nat Commun. 2022.PMCID: PMC9023578
“Programmed death-1 (PD-1) and its ligand PD-L1 are checkpoint molecules which regulate immune responses. Little is known about their functions in T cell migration and there are contradictory data about their roles in regulatory T cell (Treg) function. Here we show activated Tregs and CD4 effector T cells (Teffs) use PD-1/PD-L1 and CD80/PD-L1, respectively, to regulate transendothelial migration across lymphatic endothelial cells (LECs). Antibody blockade of Treg PD-1, Teff CD80 (the alternative ligand for PD-L1), or LEC PD-L1 impairs Treg or Teff migration in vitro and in vivo. PD-1/PD-L1 signals through PI3K/Akt and ERK to regulate zipper junctional VE-cadherin, and through NFκB-p65 to up-regulate VCAM-1 expression on LECs. CD80/PD-L1 signaling up-regulates VCAM-1 through ERK and NFκB-p65. PD-1 and CD80 blockade reduces tumor egress of PD-1high fragile Tregs and Teffs into draining lymph nodes, respectively, and promotes tumor regression. These data provide roles for PD-L1 in cell migration and immune regulation.”

4、Antibody-mediated depletion of programmed death 1-positive (PD-1+) cells
Yujia Zhai,et al.J Control Release. 2023.PMCID: PMC10699550
“PD-1 immune checkpoint has been intensively investigated in pathogenesis and treatments for cancer and autoimmune diseases. Cells that express PD-1 (PD-1+ cells) draw ever-increasing attention in cancer and autoimmune disease research although the role of PD-1+ cells in the progression and treatments of these diseases remains largely ambiguous. One definite approach to elucidate their roles is to deplete these cells in disease settings and examine how the depletion impacts disease progression and treatments. To execute the depletion, we designed and generated the first depleting antibody (D-αPD-1) that specifically ablates PD-1+ cells. D-αPD-1 has the same variable domains as an anti-mouse PD-1 blocking antibody (RMP1–14). The constant domains of D-αPD-1 were derived from mouse IgG2a heavy and κ-light chain, respectively. D-αPD-1 was verified to bind with mouse PD-1 as well as mouse FcγRIV, an immuno-activating Fc receptor. The cell depletion effect of D-αPD-1 was confirmed in vivo using a PD-1+ cell transferring model. Since transferred PD-1+ cells, EL4 cells, are tumorigenic and EL4 tumors are lethal to host mice, the depleting effect of D-αPD-1 was also manifested by an absolute survival among the antibody-treated mice while groups receiving control treatments had median survival time of merely approximately 30 days. Furthermore, we found that D-αPD-1 leads to elimination of PD-1+ cells through antibody-dependent cell-mediate phagocytosis (ADCP) and complement-dependent cytotoxicity (CDC) mechanisms. These results, altogether, confirmed the specificity and effectiveness of D-αPD-1. The results also highlighted that D-αPD-1 is a robust tool to study PD-1+ cells in cancer and autoimmune diseases and a potential therapeutic for these diseases.”

5、Macrophages Impair TLR9 Agonist Antitumor Activity through Interacting with the Anti-PD-1 Antibody Fc Domain
Simone Camelliti,et al.Cancers (Basel). 2021.PMCID: PMC8391891
“Background. A combination of TLR9 agonists and an anti-PD-1 antibody has been reported to be effective in immunocompetent mice but the role of innate immunity has not yet been completely elucidated. Therefore, we investigated the contribution of the innate immune system to this combinatorial immunotherapeutic regimens using an immunodeficient mouse model in which the effector functions of innate immunity can clearly emerge without any interference from T lymphocytes. Methods. Athymic mice xenografted with IGROV-1 human ovarian cells, reported to be sensitive to TLR9 agonist therapy, were treated with cytosine–guanine (CpG)-oligodeoxynucleotides (ODNs), an anti-PD-1 antibody or their combination. Results. We found that PD-1 blockade dampened CpG-ODN antitumor activity. In vitro studies indicated that the interaction between the anti-PD-1 antibody fragment crystallizable (Fc) domain and macrophage Fc receptors caused these immune cells to acquire an immunoregulatory phenotype, contributing to a decrease in the efficacy of CpG-ODNs. Accordingly, in vivo macrophage depletion abrogated the detrimental effect exerted by the anti-PD-1 antibody. Conclusion. Our data suggest that if TLR signaling is active in macrophages, coadministration of an anti-PD-1 antibody can reprogram these immune cells towards a polarization state able to negatively affect the immune response and eventually promote tumor growth.”

6、Distinct antibody clones detect PD-1 checkpoint expression and block PD-L1 interactions on live murine melanoma cells
Christina Martins,et al.Sci Rep. 2022.PMCID: PMC9304406
“Monoclonal antibodies (abs) targeting the programmed cell death 1 (PD-1) immune checkpoint pathway have revolutionized tumor therapy. Because T-cell-directed PD-1 blockade boosts tumor immunity, anti-PD-1 abs have been developed for examining T-cell-PD-1 functions. More recently, PD-1 expression has also been reported directly on cancer cells of various etiology, including in melanoma. Nevertheless, there is a paucity of studies validating anti-PD-1 ab clone utility in specific assay types for characterizing tumor cell-intrinsic PD-1. Here, we demonstrate reactivity of several anti-murine PD-1 ab clones and recombinant PD-L1 with live B16-F10 melanoma cells and YUMM lines using multiple independent methodologies, positive and negative PD-1-specific controls, including PD-1-overexpressing and PD-1 knockout cells. Flow cytometric analyses with two separate anti-PD-1 ab clones, 29F.1A12 and RMP1-30, revealed PD-1 surface protein expression on live murine melanoma cells, which was corroborated by marked enrichment in PD-1 gene (Pdcd1) expression. Immunoblotting, immunoprecipitation, and mass spectrometric sequencing confirmed PD-1 protein expression by B16-F10 cells. Recombinant PD-L1 also recognized melanoma cell-expressed PD-1, the blockade of which by 29F.1A12 fully abrogated PD-1:PD-L1 binding. Together, our data provides multiple lines of evidence establishing PD-1 expression by live murine melanoma cells and validates ab clones and assay systems for tumor cell-directed PD-1 pathway investigations.”

7、Targeted delivery of a PD-1-blocking scFv by CAR-T cells enhances anti-tumor efficacy in vivo
Sarwish Rafiq,et al.Nat Biotechnol. 2019.PMCID: PMC6126939
“The efficacy of CAR-T cell therapy against poorly responding tumors has been enhanced by administering the cells in combination with immune checkpoint blockade inhibitors. Alternatively, the CAR construct has been engineered to co-express factors that boost CAR-T cell function in the tumor microenvironment. Here we modified CAR-T cells to secrete PD-1-blocking single-chain variable fragments (scFv). These scFv-secreting CAR-T cells work in both a paracrine and autocrine manner to improve the anti-tumor activity of CAR-T cells and bystander tumor-specific T cells in clinically relevant syngeneic and xenogeneic mouse models of PD-L1+ hematologic and solid tumors. Efficacy was similar or better to that achieved by combination therapy with CAR-T cells and a checkpoint inhibitor. This approach could improve safety as the secreted scFv remained localized to the tumor, protecting CAR-T cells from PD-1 inhibition, which could potentially avoid toxicities associated with systemic checkpoint inhibition.

8、Type I MET inhibitors cooperate with PD-1 blockade to promote rejection of hepatocellular carcinoma
Ricardo DeAzevedo,et al.J Immunother Cancer. 2024.PMCID: PMC11529525
“Blockade of the immune checkpoints programmed death-1 (PD-1) and cytotoxic lymphocyte antigen 4 has improved outcomes for patients with hepatocellular carcinoma (HCC), yet most still fail to achieve objective clinical benefit. MET plays key roles in both HCC tumorigenesis and immunosuppressive conditioning; however, inhibition of MET causes upregulation of PD-ligand 1 (PD-L1) suggesting the use of these inhibitors in the context of PD-1 blockade. We sought to investigate across the Hepa1-6, HCA-1 and diethylnitrosamine (DEN) models of HCC whether the combination of more specific type I versus more pleiotropic type II MET inhibitors would confer superior outcomes in combination with PD-1 blockade. While MET inhibition demonstrated cooperativity with αPD-1 across all three models, the type I MET inhibitor capmatinib showed optimal activity in combination and statistically significantly outperformed the combination with the type II inhibitor cabozantinib in the αPD-1 refractory DEN model. In both HCA-1 and DEN HCC, the capmatinib and αPD-1 combination enhanced CD8 T cell frequency and activation state while limiting intratumoral myeloid immune suppression. In vitro studies of antigen-specific T cell activation reveal significantly less inhibition of effector cytokine production and proliferation by capmatinib versus by type II or type III MET inhibitors. These findings suggest significant potential for clinical HCC combination studies of type I MET inhibitors and PD-1 blockade where prior trials using type II inhibitors have yielded limited benefit.”

9、Targeting myeloid-derived suppressor cells promotes antiparasitic T-cell immunity and enhances the efficacy of PD-1 blockade
Chuanshan Zhang,et al.Nat Commun. 2024.PMCID: PMC11283557
“Immune exhaustion corresponds to a loss of effector function of T cells that associates with cancer or chronic infection. Here, our objective was to decipher the mechanisms involved in the immune suppression of myeloid-derived suppressor cells (MDSCs) and to explore the potential to target these cells for immunotherapy to enhance checkpoint blockade efficacy in a chronic parasite infection. We demonstrated that programmed cell-death-1 (PD-1) expression was significantly upregulated and associated with T-cell dysfunction in advanced alveolar echinococcosis (AE) patients and in Echinococcus multilocularis-infected mice. PD-1 blockade ex vivo failed to reverse AE patients’ peripheral blood T-cell dysfunction. PD-1/PD-L1 blockade or PD-1 deficiency had no significant effects on metacestode in mouse model. This was due to the inhibitory capacities of immunosuppressive granulocytic MDSCs (G-MDSCs), especially in the liver surrounding the parasite pseudotumor. MDSCs suppressed T-cell function in vitro in an indoleamine 2, 3 dioxygenase 1 (IDO1)-dependent manner. Although depleting MDSCs alone restored T-cell effector functions and led to some limitation of disease progression in E. multilocularis-infected mice, combination with PD-1 blockade was better to induce antiparasitic efficacy. Our findings provide preclinical evidence in support of targeting MDSC or combining such an approach with checkpoint blockade in patients with advanced AE.”

10、Immune receptor inhibition through enforced phosphatase recruitment
Ricardo A Fernandes,et al.Nature. 2021.PMCID: PMC7875542
“Antibodies that antagonize extracellular receptor–ligand interactions are used as therapeutic agents for many diseases to inhibit signalling by cell-surface receptors1. However, this approach does not directly prevent intracellular signalling, such as through tonic or sustained signalling after ligand engagement. Here we present an alternative approach for attenuating cell-surface receptor signalling, termed receptor inhibition by phosphatase recruitment (RIPR). This approach compels cis-ligation of cell-surface receptors containing ITAM, ITIM or ITSM tyrosine phosphorylation motifs to the promiscuous cell-surface phosphatase CD452,3, which results in the direct intracellular dephosphorylation of tyrosine residues on the receptor target. As an example, we found that tonic signalling by the programmed cell death-1 receptor (PD-1) results in residual suppression of T cell activation, but is not inhibited by ligand-antagonist antibodies. We engineered a PD-1 molecule, which we denote RIPR-PD1, that induces cross-linking of PD-1 to CD45 and inhibits both tonic and ligand-activated signalling. RIPR-PD1 demonstrated enhanced inhibition of checkpoint blockade compared with ligand blocking by anti-PD1 antibodies, and increased therapeutic efficacy over anti-PD1 in mouse tumour models. We also show that the RIPR strategy extends to other immune-receptor targets that contain activating or inhibitory ITIM, ITSM or ITAM motifs; for example, inhibition of the macrophage SIRPα ‘don’t eat me’ signal with a SIRPα–CD45 RIPR molecule potentiates antibody-dependent cellular phagocytosis beyond that of SIRPα blockade alone. RIPR represents a general strategy for direct attenuation of signalling by kinase-activated cell-surface receptors.”

References about Anti-mouse PD-1 antibody products，please click: anti-mouse PD–1 monoclonal antibody (clone RMP1-14) referenced literature.

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/CD279 antibody(RMP1-14.1) products from: Anti-mouse PD-1 Mouse Monoclonal Antibody PA007162.m2cLA Syd Labs

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