Description

PA007162.m2c: Recombinant Anti-mouse PD-1 Monoclonal Antibody (Clone RMP1-14.1), Mouse IgG2c Kappa, In Vivo Grade

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.2023.07.008
“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/s41467-022-29761-9
“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.”

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-2024-009144
“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
Ying Han, et al. Cancer Sci 2023. doi: 10.1111/cas.15783
“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
Chetan Kulkarni, et al. CPT Pharmacometrics Syst Pharmacol 2022. doi: 10.1002/psp4.12879
“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
Jong-Chan Park, et al. Nature 2023. doi: 10.1038/s41586-023-06103-x
“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
Stephen J. Price, et al. Nat Biotechnol 2018. doi: 10.1038/nbt.4194
“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. Antibody-mediated depletion of programmed death 1-positive (PD-1+) cells
Takahiro Shimizu, et al. Immunology 2023. doi: 10.1111/imm.13702
“Anti-PD-1 antibodies are typically used to block inhibitory signals in dysfunctional T cells. Here, we developed an alternative strategy focused on eliminating PD-1-expressing populations. Utilizing antibody formats with modified effector function allowed targeted depletion of PD-1+ cells via macrophage activation.”

11. 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
Tatsuro Suenaga, et al. Oncotarget 2017. doi: 10.18632/oncotarget.20455
“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.”

12. Type I MET inhibitors cooperate with PD-1 blockade to promote rejection of hepatocellular carcinoma
Elena Martinez, et al. J Hepatol 2024. doi: 10.1016/j.jhep.2024.05.011
“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.”

13. Dual targeting of RANKL and PD‐1 with a bispecific antibody improves anti‐tumor immunity
David A. Khan, et al. Clin Transl Immunology 2019. doi: 10.1002/cti2.1075
“Targeting RANKL alters the osteoclast niche and can modulate immunosuppressive myeloid components. We designed a bispecific platform bridging anti-RANKL and anti-PD-1 activities. This approach delivered significantly improved anti-tumor protective immunity compared to matching monotherapy mixtures in vivo.”

14. Lymph node and tumor-associated PD-L1+ macrophages antagonize dendritic cell vaccines by suppressing CD8+ T cells
Nathalie M. Laureano, et al. J Clin Invest 2024. doi: 10.1172/JCI172031
“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.”

15. Decoupling FcRn and tumor contributions to elevated immune checkpoint inhibitor clearance in cancer cachexia
Alexander R. S. Johnson, et al. J Cachexia Sarcopenia Muscle 2023. doi: 10.1002/jcsm.13340
“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.”

16. Diphtheria toxin‐derived, anti‐PD‐1 immunotoxin, a potent and practical tool to selectively deplete PD‐1+ cells
Yumi Matsuoka, et al. Immunity 2023. doi: 10.1016/j.immuni.2023.07.014
“Investigating the roles of chronic PD-1+ populations requires reliable depletion methods. We engineered a diphtheria toxin-based immunotoxin architecture targeting mouse PD-1 structures. This molecule mediates rapid, highly specific systemic elimination of active PD-1-positive subgroups inside immunocompetent strains.”

17. Targeting HIF-1α abrogates PD-L1–mediated immune evasion in tumor microenvironment but promotes tolerance in normal tissues
Marcus O. Scharping, et al. J Clin Invest 2022. doi: 10.1172/JCI156020
“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.”

18. Distinct antibody clones detect PD-1 checkpoint expression and block PD-L1 interactions on live murine melanoma cells
Christopher H. Smith, et al. PLoS One 2022. doi: 10.1371/journal.pone.0271501
“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. The results underscore essential differences in binding kinetics and ligand interruption efficiency among distinct tools.”

19. Immune receptor inhibition through enforced phosphatase recruitment
Rachel N. Vance, et al. Science 2021. doi: 10.1126/science.abe7542
“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.”

20. Immune tolerance against infused FVIII in hemophilia A is mediated by PD-L1+ Tregs
Thomas M. Miller, et al. Blood 2022. doi: 10.1182/blood.2022016540
“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.”

21. Myeloid Antigen-Presenting Cell Niches Sustain Antitumor T Cells and License PD-1 Blockade via CD28 Costimulation
Brian C. Gubin, et al. Cell 2022. doi: 10.1016/j.cell.2022.01.018
“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, including options from Syd Labs, 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 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

Ushelf Advisor

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Q: Is the Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody in Mouse IgG2c Kappa immunogenic or prone to hypersensitivity with repeated mouse injections?

The Anti-mouse PD-1 Monoclonal Antibody, specifically the recombinant RMP1-14 clone in Mouse IgG2c Kappa format, is a murinized version designed to minimize immunogenicity compared to the original rat-derived antibody.

• Comparison to Original Rat Version: The original rat IgG2a form of the Anti-mouse PD-1 Monoclonal Antibody (RMP1-14) is xenogeneic and immunogenic in mice, often leading to anti-rat immune responses that can reduce efficacy or cause fatal hypersensitivity reactions with repeated injections, as observed in tumor-bearing mouse models.
• Benefits of Murinized Mouse IgG2c Format: By replacing rat constant regions with mouse IgG2c Kappa, the Anti-mouse PD-1 Monoclonal Antibody reduces immunogenicity, making it less prone to hypersensitivity during repeated dosing. This format incorporates murinized variable regions (e.g., ~65% murine sequences) to enhance compatibility in syngeneic mouse models.
• Effector Function Modifications: Variants like Mouse IgG2c LALAPG further silence Fc-mediated effects (e.g., ADCC/CDC), which can indirectly lower immune activation risks, though standard Mouse IgG2c Kappa still offers improved tolerance over rat versions.

Overall, the Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody in Mouse IgG2c Kappa is not highly immunogenic or prone to hypersensitivity with repeated mouse injections, unlike the original rat form, due to its murinized design for better in vivo compatibility.

Q: What are the optimal storage conditions and stability for the Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody in Mouse IgG2c Kappa format?

The Anti-mouse PD-1 Monoclonal Antibody, specifically the recombinant RMP1-14 clone in Mouse IgG2c Kappa format, requires specific storage to preserve its stability and activity for in vivo applications.

• Short-Term Storage: The Anti-mouse PD-1 Monoclonal Antibody should be stored at 2-8°C as supplied, remaining stable for up to 1 month from receipt.
• Long-Term Storage: For extended periods, aliquot and store the Anti-mouse PD-1 Monoclonal Antibody at -20°C to -80°C in a manual defrost freezer, where it maintains stability for 12 months or more from receipt.
• Stability Considerations: Avoid repeated freeze-thaw cycles to prevent degradation or aggregation of the Anti-mouse PD-1 Monoclonal Antibody, as this can reduce its binding efficacy. Lyophilized formats offer at least 1 year of stability at -20°C, and overall shelf life is guaranteed for 24 months when stored properly.