Anti-Mouse PD-1 (RMP1-14) Recombinant Antibody | PA007162.m1DA

Catalog No.	PA007162.m1DA
Product Name	In Vivo Grade Recombinant Anti-mouse PD-1 Monoclonal Antibody (Clone RMP1-14.1), Mouse IgG1-D265A Kappa
Data Sheet	📄 Download Product Data Sheet (PDF)
Supplier Name	Syd Labs, Inc.
Brand Name	Syd Labs
Synonyms	Recombinant Anti-Mouse PD-1 Mouse IgG1-D265A, RMP1-14 Mouse IgG1 D265A, Recombinant RMP1-14 Antibody, Anti-Mouse PD-1 (RMP1-14) Mouse IgG1 D265A
Summary	The In Vivo Grade Recombinant Anti-mouse PD-1 Mouse IgG1-D265A 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 IgG1, 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 IgG1-D265A 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 IgG2a isotype control 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

References for Anti-mouse PD-1 (CD279, RMP1-14.1, mIgG1-D265A Fc-silent)

Below are peer-reviewed studies using the RMP1-14 anti-mouse PD-1 clone and validating PD-1 checkpoint blockade, including Fc-silent format applications. All references apply equally to PA007162.m1DA as it shares identical RMP1-14.1 variable region sequences with the clones used in these publications.

For the full reference list including Fc-effector format studies and other RMP1-14 variant publications, see the References section on the recombinant RMP1-14.1 rat IgG2a product page.

References of Anti-Mouse PD-1 Monoclonal Antibody (Clone: 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.”

2. PD-L1/PD-1 checkpoint pathway regulates hippocampal neuronal excitability and learning and memory behavior
Junli Zhao, et al. Neuron 2023. doi: 10.1016/j.neuron.2023.05.022
“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. Intraventricular administration of anti-mouse PD-1 monoclonal antibody (RMP1-14) potentiated learning and memory.”

3. PD-L1 signaling selectively regulates T cell lymphatic transendothelial migration
Wenji Piao, et al. Nat Commun 2022. doi: 10.1038/s41467-022-29930-0
“Programmed death-1 (PD-1) and its ligand PD-L1 are checkpoint molecules which regulate immune responses. 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.”

4. Macrophages Impair TLR9 Agonist Antitumor Activity through Interacting with the Anti-PD-1 Antibody Fc Domain
Simone Camelliti, et al. Cancers (Basel) 2021. doi: 10.3390/cancers13164081
“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. Fc-silent anti-PD-1 formats avoid this class of Fc-mediated off-target immunosuppression.”

5. Prophylactic IL-23 blockade uncouples efficacy and toxicity in dual CTLA-4 and PD-1 immunotherapy
Mingyi Ju, et al. J Immunother Cancer 2024. doi: 10.1136/jitc-2024-009345
“The onset of immune-related adverse events (irAEs) might serve as a clinical biomarker to predict a favorable therapeutic response to immune checkpoint inhibitors (ICIs). Moreover, in the PD-1 monotherapy cohort, patients with irAEs tended to achieve higher response rates than those lacking toxicity. Our findings fill the gap in the previous evidence that there was no correlation between irAEs and ICIs response in patients treated with anti-CTLA-4 therapy.”

6. Angiogenic inhibitor pre-administration improves the therapeutic effects of immunotherapy
Mineyoshi Sato, et al. Cancer Med 2023. doi: 10.1002/cam4.5696
“Angiogenic inhibitors combined with anti-PD-1 blockade has become a standard choice for multiple advanced malignancies. We demonstrated that pre-treatment with anti-angiogenic agents improves tumor vascular normalization. This optimal pre-administration schedule enhances the subsequent therapeutic efficacy of anti-mouse PD-1 antibody treatment in syngeneic models.”

7. 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. doi: 10.3389/fphar.2022.1056365
“Substantial inter-individual variability in response to immune checkpoint inhibition is observed clinically and in mouse models. We applied a quantitative systems pharmacology (QSP) model to investigate physiological drivers of variability. Our simulations identify critical parameters regulating anti-PD-1 efficacy and receptor occupancy profiles in murine syngeneic cohorts.”

8. Targeting PD-L2/RGMb overcomes microbiome-related immunotherapy resistance
Joon Seok Park, et al. Nature 2023. doi: 10.1038/s41586-023-06026-3
“The gut microbiota significantly influences the response of tumors to immune checkpoint blockades. We identify that a subset of commensal microbes impairs anti-PD-1 therapeutic outcomes through distinct pathways. Concurrent blockade targeting the PD-L2/RGMb axis effectively overcomes this resistance and rescues anti-PD-1 treatment efficacy.”

9. Targeted delivery of a PD-1-blocking scFv by CAR-T cells enhances anti-tumor efficacy in vivo
Sarwish Rafiq, et al. Nat Biotechnol 2018. doi: 10.1038/nbt.4195
“Combining CAR-T cells with immune checkpoint inhibitors represents an attractive strategy to counter immunosuppressive environments. We engineered CAR-T cells to locally secrete an anti-PD-1 single-chain variable fragment (scFv). This localized action achieved superior therapeutic antitumor clearance compared to systemic combination with standard anti-PD-1 antibodies.”

10. Synergistic anticancer activity of a novel oral chemotherapeutic agent containing trifluridine and tipiracil in combination with anti-PD-1 blockade in microsatellite stable-type murine colorectal cancer cells
Norihiko Suzuki, et al. Am J Cancer Res 2017. PMC: PMC5665850
“Microsatellite stable colorectal cancer displays limited response to conventional anti-PD-1 blockades. We evaluated the combined efficacy of oral trifluridine/tipiracil and systemic anti-PD-1 monoclonal antibodies. This combination significantly enhanced tumor growth inhibition and CD8+ T-cell infiltration into syngeneic lesions.”

11. Type I MET inhibitors cooperate with PD-1 blockade to promote rejection of hepatocellular carcinoma
Ricardo DeAzevedo, et al. J Immunother Cancer 2024. doi: 10.1136/jitc-2024-009690
“Hepatocellular carcinoma often creates an immune-excluded microenvironment resisting single-agent treatments. We showed that selective type I MET inhibition reverses immune exclusion patterns. Combining this targeted approach with anti-PD-1 antibody interventions triggers complete rejection in a high percentage of murine models.”

12. Lymph node and tumor-associated PD-L1+ macrophages antagonize dendritic cell vaccines by suppressing CD8+ T cells
Jenny Sprooten, et al. Cell Rep Med 2024. doi: 10.1016/j.xcrm.2023.101377
“Dendritic cell vaccinations frequently exhibit sub-optimal clinical outcomes due to local active suppression. We demonstrate that PD-L1-expressing macrophages in regional nodes directly suppress functional vaccine responses. Administering anti-PD-1 therapeutic agents effectively counteracts this macrophage-mediated antagonism.”

13. Decoupling FcRn and tumor contributions to elevated immune checkpoint inhibitor clearance in cancer cachexia
Trang T. Vu, et al. Pharmacol Res 2024. doi: 10.1016/j.phrs.2023.107048
“Cancer cachexia accelerates the clearance of multiple monoclonal therapeutic antibodies, reducing exposure. We assessed the specific contributions of target burden and FcRn-mediated recycling dynamics. Our findings outline that cachexia altered antibody elimination tracks independently of typical target receptor distributions.”

14. Targeting HIF-1α abrogates PD-L1–mediated immune evasion in tumor microenvironment but promotes tolerance in normal tissues
Christopher M. Bailey, et al. J Clin Invest 2022. doi: 10.1172/JCI150846
“Hypoxia-inducible factor 1α (HIF-1α) acts as a critical metabolic sensor regulating target expression. We show that conditional ablation of metabolic pathways selectively limits immune evasion mechanisms. Combining metabolic modulation with anti-PD-1 blockade achieves robust therapeutic responses while maintaining peripheral organ safety boundaries.”

15. 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. doi: 10.1038/s41598-022-16776-1
“Accurate characterization of receptor blockades requires precise tracking of clone specificities. We systematically evaluated multiple commercial and recombinant monoclonal antibody lines on active melanoma targets. RMP1-14 clone demonstrates high-affinity PD-1 binding and complete blockade of PD-L1 interaction, with conserved antigen recognition across Fc-engineered variants sharing identical variable regions.”

16. Immune receptor inhibition through enforced phosphatase recruitment
Ricardo A. Fernandes, et al. Nature 2020. doi: 10.1038/s41586-020-2851-2
“Inhibitory pathways typically signal via localized phosphatase clustering to disrupt downstream activation complexes. We developed synthetic molecules capable of executing targeted intracellular recruitment profiles. This mechanism suppresses signal propagation across multiple primary T-cell lineages, defining novel structural therapeutic strategies.”

17. Immune tolerance against infused FVIII in hemophilia A is mediated by PD-L1+ Tregs
Janine Becker-Gotot, et al. J Clin Invest 2022. doi: 10.1172/JCI159925
“Inhibitor development against replacement factor VIII (FVIII) represents a critical clinical challenge in hemophilia management. We demonstrated that establishing functional peripheral tolerance relies heavily on specific regulatory populations. Disrupting the pathway via anti-PD-1 administration completely breaks factor protection in experimental models.”

18. Myeloid Antigen-Presenting Cell Niches Sustain Antitumor T Cells and License PD-1 Blockade via CD28 Costimulation
Jaikumar Duraiswamy, et al. Cancer Cell 2021. doi: 10.1016/j.ccell.2021.10.008
“Intratumoral T-cell expansion and maintenance require sustained supportive micro-environments. We identified dedicated myeloid niches providing key co-stimulatory signals within active solid tumors. Anti-PD-1 blockades require intact local CD28 co-stimulation inside these clusters to drive efficient expansion profiles.”

For more technical references or data sheets regarding the Recombinant Anti-Mouse PD-1 Monoclonal Antibody (Clone: RMP1-14.1) formats, please contact our scientific support team at message@sydlabs.com.

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

Other Formats

All variants below share identical RMP1-14.1 variable region sequences and mouse PD-1 (CD279) binding specificity. They differ only in Fc isotype and Fc effector function — choose the format that matches your experimental readout and mouse strain.

Catalog No.	Isotype	Fc Effector Function	Host / Reactivity	Applications
PA007162.r2a	Rat IgG2a, kappa	Intact (ADCC / CDC competent)	Rat / Mouse	IHC, FC, in vitro and in vivo functional assays
PA007162.m2a	Mouse IgG2a, kappa	Intact (ADCC / CDC competent)	Mouse / Mouse	IHC, FC, in vitro and in vivo functional assays
PA007162.m2c	Mouse IgG2c, kappa	Intact (ADCC / CDC competent)	Mouse / Mouse	IHC, FC, in vitro and in vivo functional assays
PA007162.m1	Mouse IgG1, kappa	Low effector function	Mouse / Mouse	IHC, FC, in vitro and in vivo functional assays
PA007162.m2aLA	Mouse IgG2a-L234A L235A P329G (LALAPG), kappa	Fc-Silenced	Mouse / Mouse	IHC, FC, in vitro and in vivo functional assays, Fc-silenced neutralization
PA007162.m2cLA	Mouse IgG2c-L234A L235A P329G (LALAPG), kappa	Fc-Silenced	Mouse / Mouse	IHC, FC, in vitro and in vivo functional assays, Fc-silenced neutralization
PA007162.m1DA	Mouse IgG1-D265A, kappa	Fc-Silenced	Mouse / Mouse	IHC, FC, in vitro and in vivo functional assays, Fc-silent neutralization
PA007162.mm2cLA	Fully murinized mouse IgG2c-LALAPG, kappa	Fc-Silenced	Mouse / Mouse	Long-term in vivo studies, minimal anti-drug antibody response
PA007162.rt	Rabbit IgG	Rabbit Fc (non-mouse effector)	Rabbit / Mouse	IHC, FC, in vitro and in vivo functional assays

How to choose a format for Fc-silenced studies: PA007162.m1DA (D265A) is our most widely used Fc-silent format, suitable for both BALB/c and C57BL/6 backgrounds. For C57BL/6 models (MC38, B16-F10), mouse IgG2c-LALAPG (m2cLA/mm2cLA) provides minimal anti-drug antibody response during long-term repeat dosing. If your readout requires Fc-mediated PD-1+ cell depletion, use the intact Fc format PA007162.r2a (Rat IgG2a).

Ushelf Advisor

AI-generated answers, based on peer-reviewed literature and Ushelf product data. This section is provided as a research reference. Please verify critical parameters — dosing, working dilutions, buffer conditions — against the primary references, or confirm with our technical support before finalizing an experimental design. Last updated: October 2026.

Q: What is the key advantage of the D265A Fc-silent format compared to wild-type Rat IgG2a RMP1-14?

The D265A Fc-silent format provides distinct functional advantages for long-term repeat dosing and mechanistic studies by eliminating unwanted immune effector functions while preserving target blockade.

• Effector Function Elimination: The D265A mutation in the mouse IgG1 Fc region abrogates Fcγ receptor binding and eliminates ADCC/CDC effector functions.
• Retained Target Activity: It retains full PD-1 binding and blockade activity, ensuring uncompromised pathway inhibition.
• Experimental Benefits: This allows pure PD-1 pathway inhibition without Fc-mediated depletion of PD-1-expressing cells, significantly reducing off-target effects and experimental confounders in long-term repeat dosing studies.

Q: Is m1DA recommended for C57BL/6 or BALB/c mouse strains?

The PA007162.m1DA antibody is versatile and can be utilized across different common mouse genetic backgrounds, with specific options available to optimize compatibility.

• Broad Efficacy: PA007162.m1DA works effectively in both C57BL/6 and BALB/c strains.
• C57BL/6 Models: For C57BL/6 background models (e.g., MC38, B16-F10) where IgG2c is the natural isotype, researchers may also consider PA007162.m2cLA (LALAPG Fc-silent) for reduced anti-drug antibody responses.
• BALB/c Models: For BALB/c models (e.g., CT26), m1DA works optimally.

Q: Is this antibody validated for in vivo use?

Yes, this antibody is rigorously tested and confirmed to meet stringent criteria required for preclinical in vivo applications.

• Quality Specifications: Each lot is released against in vivo grade specifications: purity greater than 95% by SDS-PAGE under reducing conditions, endotoxin less than 1.0 EU/mg by LAL method, sterility tested, animal-free, azide-free, and carrier-protein-free.
• Functional Validation: It is functionally validated for PD-1 blockade in syngeneic mouse tumor models.

Q: Can this Fc-silent antibody be used in studies where Fc-mediated depletion of PD-1+ cells is desired?

No, the Fc-silent design specifically precludes applications that rely on immune cell depletion via effector functions.

• Depletion Limitation: If your experimental readout requires Fc-mediated PD-1+ cell depletion, this Fc-silent format is unsuitable.
• Alternative Format: Researchers should use the wild-type Fc format PA007162.r2a (Rat IgG2a) instead when depletion is desired.
• Design Purpose: m1DA is specifically engineered for studies that require clean PD-1 blockade without effector function confounders.

Q: How does the affinity and blocking ability of Recombinant Anti-mouse PD-1 Antibody RMP1-14 compare to other clones?

The Recombinant Anti-mouse PD-1 Antibody RMP1-14 is a widely used clone for in vivo PD-1 blockade in mouse models, but literature comparisons highlight differences in affinity and blocking potency relative to other clones like 29F.1A12 and J43.

• Affinity: Studies show that the Recombinant rmp1-14 antibody binds to mouse PD-1 with an apparent affinity of approximately 28.8 nM, which is about 100-fold weaker than the 0.42 nM affinity of clone 29F.1A12. Clone J43 exhibits intermediate binding strength, though direct quantitative comparisons to RMP1-14 are less detailed, often placing it between 29F.1A12 and RMP1-14 in overall avidity.
• Blocking Ability: The Recombinant Anti-mouse PD-1 Antibody RMP1-14 effectively blocks PD-1 binding to PD-L1 and PD-L2, with IC50 values of 3.23 μg/mL and 4.05 μg/mL, respectively, but requires higher concentrations than 29F.1A12 (IC50 of 0.036 μg/mL for PD-L1 and 0.034 μg/mL for PD-L2), again indicating ~100-fold lower potency. Compared to J43, RMP1-14 shows similar or slightly stronger blocking in some assays, though both are outperformed by 29F.1A12 in reversing PD-1-mediated T-cell inhibition. Notably, RMP1-14 also displays dual functionality with some agonist activity at high PD-1 expression levels, unlike the pure blocking profile of 29F.1A12.

Overall, while the Recombinant Anti-mouse PD-1 Antibody RMP1-14 is effective for PD-1 blockade, 29F.1A12 is generally superior in affinity and blocking efficiency, making it a closer surrogate for high-affinity human PD-1 therapeutics. Researchers may prefer RMP1-14 for scenarios requiring moderate-affinity binding to target high-PD-1-expressing tissues.

Q: Is Recombinant Anti-mouse PD-1 Antibody RMP1-14 immunogenic or prone to hypersensitivity in repeated mouse injections?

The Recombinant Anti-mouse PD-1 Antibody RMP1-14, originally derived from a rat hybridoma, has been associated with immunogenicity concerns in its non-murinized form, but recombinant versions are designed to mitigate these issues.

• Immunogenicity of Original Rat-Derived Version: The rat-origin sequences in the original Recombinant rmp1-14 antibody render it immunogenic upon injection in mice, often triggering host anti-rat immune responses that can compromise antibody performance or lead to immunogenic events with repeated administrations. This is particularly noted for PD-1/PD-L1 axis-targeting antibodies, where repeated injections in tumor-bearing mice have induced fatal xenogeneic hypersensitivity reactions.
• Hypersensitivity Risks: In a murine model of breast cancer, repeated administration of xenogeneic (rat-derived) Recombinant Anti-mouse PD-1 Antibody RMP1-14 led to fatal hypersensitivity, highlighting the risks in syngeneic tumor models with multiple doses. These reactions are attributed to the foreign rat sequences provoking immune responses.
• Mitigation in Recombinant Murinized Formats: To address these issues, recombinant versions like the Mouse IgG1-D265A Kappa (In Vivo Grade) of Recombinant Anti-mouse PD-1 Antibody RMP1-14 incorporate murinized variable regions and mouse constant regions, reducing immunogenicity and hypersensitivity risks. For instance, fully murine or murinized clones show improved survival and tumor regression compared to the original RMP1-14 in repeated dosing scenarios, with lower rates of adverse immune reactions.

Overall, while the original rat-derived Recombinant rmp1-14 antibody is prone to immunogenicity and hypersensitivity in repeated mouse injections, the recombinant Mouse IgG1-D265A version is engineered for reduced risks, making it more suitable for in vivo studies.