重组抗小鼠PD-1抗体 (RMP1-14.1) | Syd Labs PA007162.r2a
Syd Labs 重组抗小鼠 PD-1 单克隆抗体 (克隆号: RMP1-14.1, 货号: PA007162.r2a) 采用哺乳动物细胞重组表达，与经典 RMP1-14 克隆具有完全相同的可变区序列。专为体内（In Vivo）PD-1/PD-L1 通路阻断及免疫检查点研究设计，批次间高度稳定，提供极高性价比。
- 应用范围： 适配体内阻断（In Vivo Blocking）、流式细胞术（FC）、免疫组化（IHC）及体外功能分析。
- 亚型与对照： 大鼠 IgG2a Kappa (rIgG2a)，可与重组大鼠IgG2a同型对照抗体（Isotype Control）配套使用。
- 品质保障： 严格控制内毒素水平（≤0.05 EU/mg 或 ≤1 EU/mg），无杂交瘤基因突变及批次间差异，现货供应。
💡 实验参考指南：
• 剂量参考：RMP1-14抗体在不同小鼠肿瘤模型中剂量建议
• 应用指南：抗小鼠PD-1单抗（RMP1-14）如何用于体内PD-1阻断研究
产品参数
| 货号 | PA007162.r2a |
|---|---|
| 产品名称 | 重组抗小鼠PD-1抗体 (RMP1-14.1) | Syd Labs PA007162.r2a |
| 英文名 | In Vivo Grade Recombinant Anti-mouse PD-1 Monoclonal Antibody (Clone RMP1-14.1), Rat IgG2a Kappa |
| 供货商名称 | Syd Labs, Inc. |
| 品牌名 | Syd Labs |
| 别称 | CD279 |
| 概述 | 重组抗小鼠PD-1（CD279）单克隆抗体的可变区序列是从大鼠抗小鼠PD-1单抗(克隆号:RMP1-14)中提取的。重组大鼠和嵌合小鼠版本的RMP1-14抗体也可用。 |
| 克隆号 | RMP1-14.1，与大鼠抗小鼠PD1单克隆抗体（克隆号：RMP1-14）的可变区和不变区序列相同。 |
| 同种型 | 大鼠 IgG2a, kappa |
| 应用 | 免疫组织化学(IHC)，流式细胞术(FC)，以及各种体外和体内功能分析。 |
| 免疫源 | 原大鼠杂交瘤(克隆号:RMP1-14)是用小鼠pd -1转染的BHK细胞免疫大鼠产生的。 |
| 抗体形式 | 0.2 μM过滤溶液，1x PBS |
| 内毒素 | 根据 LAL 方法，≤1 EU每1mg 蛋白质。提供特级体内实验级重组抗小鼠PD 1单克隆抗体，大鼠IgG2a Kappa（RMP1-14.1）（内毒素≤0.05 EU/mg)。 |
| 纯度 | >95%（在还原条件下通过SDS-PAGE测定） |
| 运输 | 体内实验级重组抗小鼠PD-1（CD279)单克隆抗体（克隆号RMP1-14.1），大鼠IgG2a Kappa用冰袋运输。收到后，请立即将其存放在下面建议的温度下。 |
| 稳定性与存储 | 抗小鼠PD-1单抗使用手动除霜冰箱并避免重复冻融循环。 如果保存在2 至 8°C，自收到之日起可保存1个月。 如果保存在-20 至 -70°C，自收到之日起可保存 12个月。 |
| 应用详情 | 抗小鼠pd-1抗体用于免疫组织化学(IHC)，流式细胞术(FC)，以及各种体外和体内功能分析。 |
文献
PA007162.r2a：Syd Labs重组抗小鼠PD-1抗体（RMP1-14.1）
大鼠抗小鼠 PD-1 单克隆抗体（克隆号：RMP1-14.1，Rat IgG2a $\kappa$）可与小鼠 PD-1 蛋白（CD279 或程序性死亡受体 1）发生特异性反应。该蛋白由小鼠 *pdcd1* 基因编码，属于免疫球蛋白超家族（Ig superfamily）中的 CD28 家族成员。PD-1 拥有 PD-L1 和 PD-L2 两个配体，二者均属于 B7 家族。研究表明，在黑色素瘤和结肠癌的小鼠模型中，通过抗小鼠 PD-1 抗体治疗以及抗小鼠 PD-L1 抗体干预来阻断 PD-L1 蛋白与其受体 PD-1 蛋白之间的相互作用，可使肿瘤生长受到暂时的抑制。在体内检查点阻断实验中，RMP1-14.1 阻断型抗体能有效阻断小鼠 PD-L1 蛋白与小鼠 PD-L2 蛋白向小鼠 PD-1 蛋白的相互结合。
我们的重组 RMP1-14.1 抗体采用了源自原始大鼠杂交瘤（克隆号：RMP1-14）可变区的 100% 精确氨基酸序列进行基因工程重组。该体内级（In Vivo Grade）重组抗小鼠 PD-1 抗体采用先进的哺乳动物细胞表达，具备卓越的批间一致性，结合亲和力低于 2 nM（$K_D < 2\text{ nM}$），纯度大于 95%。产品提供多种灵活的格式选择，包括经典的 Rat IgG2a 以及 Fc 沉默型 Mouse IgG2c LALAPG（L234A/L235A/P329G）平台；采用低内毒素（$< 1\text{ EU/mg}$）、不含叠氮化物（Azide-free）的配方设计，可彻底消除非特异性细胞激活，是免疫组化（IHC）、流式细胞术（FC）、体外中和实验（In Vitro Neutralization）以及长期体内功能学实验的理想选择。
重组抗小鼠PD-1单抗（克隆号：RMP1-14.1）引用文献:
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.”
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.”
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.”
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.”
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.”
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.”
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.”
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.”
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.”
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.”
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.”
重组抗小鼠 PD-1 单抗 (克隆号: RMP1-14.1) 常见问题解答 (FAQ)
问: 与杂交瘤来源的抗体相比，重组 RMP1-14.1 抗体有哪些优势？
答：传统杂交瘤来源的抗体常面临杂交瘤基因漂移和批次间差异的问题，这会严重破坏长期临床前研究的重复性。我们的重组抗小鼠 PD-1 抗体（克隆号 RMP1-14.1）采用 100% 经验证的基因序列构建，并在先进的哺乳动物细胞培养体系中表达。这确保了绝对的序列完整性、卓越的批次间重复性以及可扩展的生产能力。在严格的质量控制下纯化的体内级重组 RMP1-14.1 具有高结合亲和力和超高纯度，能提供完全不受杂交瘤相关细胞污染物干扰的清爽、可靠数据。
问: 针对我的小鼠模型研究，我应该选择哪种重组 RMP1-14.1 的工程化同种型或格式？
答：Syd Labs 为克隆号 RMP1-14.1 提供了 8 种灵活的重组工程化格式，量身定制以匹配特定小鼠品系和功能需求，从而防止免疫原性和抗药物抗体（ADA）反应：
标准基础对照： Rat IgG2a Kappa (PA007162.r2a) 与原始杂交瘤格式一致，广泛用于经典的短期体内检查点阻断实验。
适用于 C57BL/6、C57BL/10 或 NOD 背景（Fc 沉默型）： 强烈推荐 Mouse IgG2c LALAPG Kappa (PA007162.m2cLA)。由于这些品系表达 IgG2c 等位基因而非 IgG2a，使用 Fc 沉默的小鼠 IgG2c LALAPG 骨架可完全消除抗体依赖性细胞毒性（ADCC），并在慢性给药期间最大限度地降低免疫原性。
适用于 BALB/c、C3H 或 DBA/2 背景（Fc 沉默型）： 应选择 Mouse IgG2a LALAPG Kappa (PA007162.m2aLA)，以完美匹配这些品系天然的 IgG2a 表达，同时提供 Fc 沉默特性。
替代型 Fc 沉默平台： Mouse IgG1 D265A Kappa (PA007162.m1DA) 引入了经典的 D265A 单点突变以消除 Fc 受体结合，确保与历史基准数据集保持连续性。
天然低效应子特性（未经改造）： 野生型 Mouse IgG1 Kappa (PA007162.m1) 提供天然、未经改造的小鼠骨架，相比 IgG2a/IgG2c，其对激活型 Fc 受体的结合亲和力天然显著降低，为特定生理学测定提供了理想的基线。
用于效应子功能与 T 细胞清除： 野生型 Mouse IgG2a Kappa (PA007162.m2a) 和 Mouse IgG2c Kappa (PA007162.m2c) 保留了强大的 ADCC 和 CDC 能力，是实现清除机制或靶向耗竭测定而非纯粹阻断的理想选择。
跨物种与特殊测定： Rabbit IgG (PA007162.rt) 经工程化设计，专用于独特的跨物种桥接或非啮齿类动物的免疫组化配置。
问: 重组 RMP1-14.1 的典型体内半衰期是多少？小鼠的推荐给药频率如何？
答：在标准免疫健全的小鼠中，我们的重组嵌合小鼠格式（如小鼠 IgG2c LALAPG 和 IgG2a 变体）的体内半衰期为 5 至 8 天，表现出优于异源大鼠宿主骨架的卓越稳定性。对于已建株的同源小鼠肿瘤模型（如 MC38、CT26 或 B16），标准验证的体内给药方案为每只小鼠 100 $\mu\text{g}$ 至 200 $\mu\text{g}$，每 3 至 4 天（每周两次）通过腹腔注射（i.p.）给药一次。治疗通常在可触及的皮下肿瘤平均体积达到 50–100 $\text{mm}^3$ 时开始。
问: 为了避免实验人为误差，在使用重组 RMP1-14.1 时应搭配哪种同型对照？
答：为了从体内免疫检查点阻断实验中获得可靠且可用于发表的数据，您的阴性对照必须与靶向抗体精确匹配相同的工程化骨架和突变。如果您使用的是天然平台 (PA007162.r2a)，请搭配重组 Rat IgG2a 同型对照。至关重要的是，如果您的研究使用了特殊格式，如 Mouse IgG2c LALAPG (PA007162.m2cLA)、Mouse IgG2a LALAPG (PA007162.m2aLA)、Mouse IgG1 D265A (PA007162.m1DA) 或野生型 Mouse IgG1 (PA007162.m1)，使用通用型或不匹配的同型对照会引入严重的背景 Fc 受体激活差异，从而使您的实验结果彻底失效。您必须将它们与各自精确对应的重组小鼠同型对照（例如 Syd Labs 货号 PA007141 变体）进行配对。
问: Syd Labs 的重组 RMP1-14.1 在纯度、内毒素水平、适用应用及储存指南方面的标准是什么？
答：我们的体内级重组抗小鼠 PD-1 抗体专为敏感的生理环境配制。产品以 0.2 $\mu\text{m}$ 过滤的 1x PBS 溶液形式提供，完全无叠氮化物且无防腐剂，以保证体内或体外无细胞毒性。通过 LAL 方法测定，内毒素水平严格保持在每毫克蛋白质小于 1 EU（$< 1\text{ EU/mg}$）。虽然它被优化为小鼠同源肿瘤模型中的强效功能性阻断剂，但其高度特异性使其完全兼容流式细胞术（FC）、免疫组化（IHC）和体外 T 细胞中和实验。短期使用可储存在 2–8°C，或分装后储存在 -20°C 至 -70°C 下，保存期长达 12 个月。