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Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody | PA007162.rt

Name: Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody | Ushelf
Brand: Syd Labs
SKU: PA007162.rt
Price: 595 USD
Availability: InStock
Rating: 5 (12 reviews)

$595.00

In Vivo Grade Recombinant Anti-mouse PD-1 Rabbit IgG Monoclonal Antibody (Clone RMP1-14.1). 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.

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Syd Labs, Inc.

SKU: PA007162.rt Categories: Anti-Mouse Antibodies (In Vivo), Antibodies Tags: Anti-mouse CD279 In Vivo Antibody, Anti-mouse PD-1, Anti-mouse PD-1 Antibody

Details & Specifications
References
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Catalog No.	PA007162.rt
Name	Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody \| PA007162.rt
Product Name	In Vivo Grade Recombinant Anti-mouse PD-1 Monoclonal Antibody (Clone RMP1-14.1), Rabbit IgG
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 Rabbit IgG Monoclonal Antibody (Clone RMP1-14.1) was produced in mammalian cells.
Clone	RMP1-14.1, the same variable region and constant region sequences as the rat anti-mouse PD-1 monoclonal antibody (clone number: RMP1-14)
Isotype	Rabbit IgG, 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 Sprague Dawley rats with mouse PD-1-transfected BHK cells and using a P3U1 myeloma as the fusion partner.
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 Rabbit IgG 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.rt: Recombinant Anti-mouse PD-1 Monoclonal Antibody (RMP1-14.1), Rabbit IgG kappa, In Vivo Grade

The rat anti-mouse PD-1 monoclonal antibody (clone No. RMP1-14.1, rat IgG2a kappa) reacts with the mouse PD-1 protein (CD279 or programmed death-1) encoded by the mouse pdcd1 gene, a member of the CD28 family of the Ig superfamily. PD-1 has two ligands, PD-L1 and PD-L2, both of which belong to the B7 family. It has been shown that in mouse models of melanoma and colon cancer, tumor growth can be transiently arrested via anti-mouse PD-1 antibody treatment and anti-mouse PD-L1 antibody interventions which block the therapeutic interaction between the PD-L1 protein and its receptor PD-1 protein. The RMP1-14.1 blocking antibody effectively blocks the reciprocal binding of both the mouse PD-L1 protein and the mouse PD-L2 protein to the mouse PD-1 protein during in vivo checkpoints blocking.

Our recombinant RMP1-14.1 antibody is engineered with 100% precise amino acid sequences of the variable regions derived from the original rat hybridoma (clone: RMP1-14). Expressed in advanced mammalian cells, this in vivo grade recombinant anti-mouse PD-1 antibody delivers superior batch-to-batch consistency with a high binding affinity <2 nM and purity >95%. Available in versatile formats including the classic rat IgG2a and the Fc-silent mouse IgG2c LALAPG (L234A/L235A/P329G) platforms, this low endotoxin (<1 EU/mg), azide-free formulation eliminates non-specific cell activation, making it ideal for immunohistochemistry (IHC), Flow Cytometry (FC), in vitro neutralization, and long-term in vivo functional assays.

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.”

Related Recombinant IgG Reference Antibodies:

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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

Ushelf Advisor

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Q: Is there an Fc-silenced variant of the Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody available in Rabbit IgG?

Based on supplier data and product specifications, the Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody is available in Rabbit IgG format, but no Fc-silenced variants (e.g., with D265A or LALAPG mutations) are commercially offered in this isotype.

Standard Rabbit IgG Availability: The Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody in Rabbit IgG (e.g., chimeric or recombinant) is produced by suppliers like Syd Labs (catalog PA007162.rt) and Ushelf, with applications in IHC, FC, and in vivo assays, but without Fc-silencing mutations.
Fc-Silenced Alternatives: Fc-silenced versions of the Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody exist in mouse isotypes, such as Mouse IgG1-D265A (effectorless, from InvivoGen and Syd Labs) and Mouse IgG2a Fc Silent™, designed to eliminate ADCC/CDC for in vivo studies.
No Rabbit IgG Fc-Silenced Option: While reformatting services (e.g., from Absolute Antibody) allow custom engineering into Rabbit IgG, no pre-made Fc-silenced Rabbit IgG variant is listed, as silencing mutations are primarily applied to mouse Fc regions for reduced immunogenicity in murine models.

Q: How does the affinity and blocking ability of the Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody in Rabbit IgG compare to higher-affinity clones?

The Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody in Rabbit IgG format shares the variable region of the RMP1-14 clone, which is commonly compared to higher-affinity clones like 29F.1A12 and J43 in literature for PD-1/PD-L1 blockade in mouse models.

Affinity: The Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody binds mouse PD-1 with an apparent affinity of approximately 28.8 nM, which is ~100-fold weaker than the 0.42 nM affinity of clone 29F.1A12. Clone J43 shows intermediate affinity, generally between RMP1-14 and 29F.1A12, though quantitative data is less precise.
Blocking Ability: The Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody effectively blocks PD-1 interaction with PD-L1 and PD-L2, with IC50 values of 3.23 μg/mL for PD-L1 and 4.05 μg/mL for PD-L2, but it is ~100-fold less potent than 29F.1A12 (IC50 of 0.036 μg/mL for PD-L1 and 0.034 μg/mL for PD-L2). Compared to J43, RMP1-14 offers similar or slightly better blocking in some assays, but both are outperformed by 29F.1A12 in reversing T-cell inhibition. RMP1-14 also exhibits partial agonist activity at high PD-1 levels, unlike the pure blocking profile of 29F.1A12.

Overall, while the Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody in Rabbit IgG is suitable for PD-1 blockade, 29F.1A12 is superior in affinity and potency, serving as a better surrogate for high-affinity human PD-1 therapeutics. The Rabbit IgG format does not alter these intrinsic clone properties but may influence immunogenicity in vivo.

Ship from Country	USA
Size	5 mg Clear

Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody | PA007162.rt

Anti-Mouse PD-1 (CD279) [RMP1-14] In Vivo Antibody | PA007162.rt