Description

Recombinant Anti-mouse PD-1 (CD279) Antibody – Clone RMP1-14.1: The Precision Evolution of RMP1-14

The Recombinant Anti-mouse PD-1 Monoclonal Antibody (Clone RMP1-14.1) represents the next generation of checkpoint inhibitors for immunotherapy research. As a sequence-defined, recombinant version of the classic RMP1-14 clone, RMP1-14.1 is engineered to eliminate the inherent variability of hybridoma-derived antibodies, providing researchers with 100% batch-to-batch consistency and superior molecular integrity.

Targeting the CD279 (Programmed Death-1) receptor, this antibody is specifically optimized for in vivo PD-1 blockade in syngeneic mouse models. Unlike traditional RMP1-14, our recombinant RMP1-14.1 is produced in a specialized mammalian expression system, ensuring it is animal-free, ultra-pure, and carries the precise in vivo functional grade required for high-impact preclinical studies.

Why RMP1-14.1 is the New Gold Standard:

• Engineered for Reproducibility: Being sequence-defined, RMP1-14.1 eliminates the risk of “gene loss” often seen in hybridoma cell lines, guaranteeing identical performance across every vial.

• Validated for Tumor Models: Extensively tested in MC38, CT26, and B16-F10 syngeneic models to ensure potent neutralization of the PD-1/PD-L1 axis.

• Advanced Fc-Engineering: Available in multiple formats, including Rat IgG2a, Mouse IgG1/IgG2a, and Fc-silent (LALAPG) mutations to minimize non-specific Fc-receptor binding during sensitive T-cell exhaustion studies.

Unlike traditional RMP1-14 hybridomas which are prone to genetic drift and lot-to-lot variation, Syd Labs’ Recombinant RMP1-14.1 is sequence-defined. This ensures that the antibody you use in 2026 will perform exactly the same as the batch you used five years ago. For researchers performing T-cell activation assays alongside checkpoint inhibition, this antibody is the ideal companion to Syd Labs’ Recombinant OKT3 (Anti-human CD3) and other effector-cell modulators.

Citations: This recombinant clone is gaining rapid traction as a high-reproducibility alternative to hybridoma-derived BE0146.

References about Anti-mouse PD-1 (CD279, RMP1-14.1) MAb，please click: anti-mouse PD-1 monoclonal antibody (clone RMP1-14) referenced literature.

Citations of Syd Labs Anti-mouse (CD279) PD-1 (RMP1-14.1):

1、Spermidine potentiates anti-tumor immune responses and immunotherapy sensitivity in breast cancer
Xinyu Yang,et al.J Cancer 2025.doi:10.7150/jca.113235
“In vivo spermidine supplementing experiment：To establish a subcutaneous tumor-bearing mouse model …… Docetaxel (Sanofi Mature IP) was administered intraperitoneally at 10 mg/kg one week after tumor inoculation in mice, followed by a single intraperitoneal injection of PD-1 antibody (SYD, PA007162) at a dosage of 10 mg/kg …… The Institutional Animal Care and Use Committee at Sun Yat-Sen University granted approval for animal experiments. ”

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. 2023.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.”
Tags: anti-mouse PD-1 RMP1-14; anti-mouse PD-1 RMP1-14 mAb

2、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.”
Tags: anti-mouse PD-1 RMP1-14 antibody in animal model; anti-mouse PD-1 RMP1-14 mAb in animal model

3、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
“Simple Summary: We evaluated the contribution of macrophages to the effect of combinatorial immunotherapeutic treatments based on TLR9 stimulation (with CpG-ODNs) and PD-1 blockade in an ovarian cancer preclinical model. We observed a strong reduction in the antitumor efficacy of a TLR9 agonist upon anti-PD-1 antibody administration. Specifically, we found that TLR9-stimulated macrophages, through interacting with the fragment crystallizable (Fc) domain of the anti-PD-1 antibody, acquire an immunoregulatory phenotype leading to dampening of CpG-ODN antitumor effect. Since the stimulation of macrophage TLRs can be achieved not only by synthetic agonists but also by molecules present in the tumor microenvironment, the data we are presenting may represent another possible mechanism of anti-PD-1 antibody therapy resistance. Indeed, it is possible that when delivered as a monotherapy, anti-PD-1 antibody Fc domain may interact with macrophages in which TLR signaling has already been triggered by endogenous ligands, mirroring the biological effects described in the present study. Abstract: 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.”
Tags: anti-mouse PD-1 RMP1-14 in cancer research; anti-mouse PD-1 RMP1-14 mAb in cancer research

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

Ushelf Advisor

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Q: What is the recommended in vivo dosage for anti-mouse PD-1 antibody in tumor models?

There is no single universally “recommended” dosage for anti-mouse PD-1 antibodies (e.g., clone RMP1-14, the most widely used) in syngeneic tumor models, as it varies based on factors like tumor type (e.g., MC38, B16, CT26), mouse strain (commonly C57BL/6), timing relative to tumor inoculation, combination therapies, and desired effect (pure blockade vs. partial depletion).
However, based on extensive use in published studies and other supplier guidelines, the most common regimens are:

Dose per injection: 200–500 μg per mouse (typically ~10–25 mg/kg for a 20–25 g mouse). The lower end (200–250 μg or ~10 mg/kg) is most frequently reported for effective PD-1 blockade with minimal toxicity in responsive models.

Frequency and schedule: Every 3–5 days, often for 3–6 doses total. A classic protocol is injections on days 3, 6, 9 (or similar) post-tumor implantation, with additional doses as needed.
Route of administration: Intraperitoneal (i.p.) injection is standard.

Q: Which anti-mouse PD1 antibody works the best?

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).

Q: Do you produce any recombinant Fc-silenced RMP1-14 antibody?

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.

Q: What is the difference among PA007162.r2a, PA007162.m2cLA, and PA007162.mm2cLA?

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.