REGN2878
Based on 1 Customer Validation
REGN2878 (PRLR ADC antibody) is a monoclonal antibody targeting the prolactin receptor (PRLR) and can block prolactin‑mediated activation of PRLR. REGN2878 exhibits an equilibrium dissociation constant (KD) of 1.05 nM and an IC50 of 0.344 nM for human PRLR. REGN2878 can be rapidly internalized and degraded in lysosomes by PRLR‑positive tumor cells, showing antigen‑specific binding and targeted enrichment properties. REGN2878 derivatives can be used as an immunoPET agent for antigen‑specific imaging of PRLR‑related tumors, and can also serve as a component of ADCs to exert anti‑tumor activity in breast cancer xenograft models. REGN2878 can be used in the research of breast cancer and prostate cancer. Isotype Comparison HY-P99001.
For research use only. We do not sell to patients.
- Purity : 95.61%
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Isotype
Human IgG1 kappa
Recommend Isotype Controls
Species Reactivity
Human
In Vitro
REGN2878 (3.125-200 nM) binds human monomeric PRLR with high affinity (Kd = 1.05 nM) and monkey monomeric PRLR with similar high affinity, but does not bind rodent PRLR[1].
REGN2878 (520 pM-30 nM; 1 h) inhibits the binding of human PRLR to its ligand PRL in an ELISA-based assay with an IC50 of 5.0 nM[1].
REGN2878 (3.38 pM-200 nM; 5 h) potently inhibits PRL-induced PRLR-STAT5 signaling in engineered HEK293 reporter cells with an IC50 of 0.4 nM[1].
REGN2878 binds to cell surface PRLR on MCF7, MCF7/PRLR, and T47D breast cancer cell lines, with binding intensity correlating with PRLR expression levels[1].
REGN2878 potently inhibits 131I REGN2878 binding to MCF-7/PRLR cells with IC50 values of 0.344 nM (parental) and 0.3343 nM (127I-labeled), respectively, while DFO-conjugated REGN2878 shows a ratio-dependent increase in IC50[2].
REGN2878 (6.25-200 nM) binds human PRLR ectodomain with a Kd of 4.20 nM, and DFO-conjugated REGN2878 shows minimal ratio-dependent decreases in binding affinity[2].
REGN2878 (60 min) retains high immunoreactivity (67-120%) for PRLR expressed on MCF-7/PRLR cells[2].
REGN2878 specifically binds human PRLR ectodomain protein[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
When labeled with 89Zr (522 kBq-5.51 MBq (4.7-24 μg); intravenous injection; single dose), REGN2878 achieves specific tumor uptake in a low PRLR-expressing MCF-7 breast cancer xenograft model in female athymic nude mice[2].
89Zr-labeled REGN2878 (503 kBq-5.51 MBq (4.6-24 μg), with 2 mg of non-radioactive REGN2878; intravenous injection; single dose) achieves specific, blockable tumor uptake in the PC3/PRLR prostate cancer xenograft model of male CB17 SCID mice. Pre-administration of 2 mg non-radioactive REGN2878 reduces the uptake to 10.2 %IA/g at ~48 h[2].
When labeled with 89Zr (522 kBq-5.51 MBq, 4.7-24 μg, single intravenous dose), REGN2878 shows low tumor uptake in the PC3 prostate cancer xenograft model with extremely low PRLR expression in male CB17 SCID mice, while it achieves specific tumor uptake in the T47Dv11 breast cancer xenograft model with moderate PRLR expression in female CB17 SCID mice[2].
When labeled with 124I (4.81 MBq (34.2 μg); intravenous injection; single dose), REGN2878 exhibits extremely low tumor uptake and rapid systemic clearance in the MCF-7/PRLR breast cancer xenograft model of female athymic nude mice[2].
After labeling with 124I (725 kBq; intravenous injection; single co-injection), REGN2878 shows extremely low and continuously decreasing tumor uptake in MCF-7/PRLR breast cancer xenografts of female athymic nude mice, whereas 89Zr-REGN2878 (181 kBq; intravenous injection; single co-injection) exhibits high and continuously increasing tumor uptake[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:athymic nude mice (female)[2]
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Dosage:522 kBq (4.7 μg) Zr-89 REGN2878 (biodistribution studies)
5.51 MBq (24 μg) Zr-89 REGN2878 (imaging studies) -
Administration:i.v.; single dose (biodistribution studies)
i.v.; single dose (imaging studies) -
Result:Reached a mean of 40.0%IA/g at 138 h post-injection.
Showed a mean tumor uptake of 16.4%IA/mL at ~140.8 h post-injection via imaging.
Exhibited low normal organ uptake, similar to uptake in mice with MCF-7/PRLR xenografts.\nReached a mean of partial tumor uptake data at 138 h post-injection, with full results incomplete.
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Animal Model:CB17 SCID mice (male)[2]
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Dosage:522 kBq (4.7 μg) Zr-89 REGN2878 (standard biodistribution studies)
5.51 MBq (24 μg) Zr-89 REGN2878 (imaging studies)
2 mg nonradioactive REGN2878 + 503 kBq (4.6 μg) Zr-89 REGN2878 (blocking studies) -
Administration:i.v.; single dose (standard biodistribution studies)
i.v.; single dose (imaging studies)
i.v.; single dose (blocking studies) -
Result:Reached a mean of 27.1%IA/g at 138 h post-injection without pre-blocking.
Showed a mean tumor uptake of 27.4%IA/mL at ~143 h post-injection via imaging.
Reduced tumor uptake to a mean of 10.2%IA/g at ~48 h post-injection with pre-administration of 2 mg nonradioactive REGN2878, while unblocked tumor uptake at ~48 h post-injection was a mean of 25.2%IA/g.
Exhibited blocked tumor uptake similar to uptake in low PRLR-expressing PC3 xenografts.
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Animal Model:CB17 SCID mice (male)[2]
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Dosage:522 kBq (4.7 μg) Zr-89 REGN2878 (biodistribution studies)
5.51 MBq (24 μg) Zr-89 REGN2878 (imaging studies) -
Administration:i.v.; single dose (biodistribution studies)
i.v.; single dose (imaging studies) -
Result:Reached a mean of 7.6%IA/g at 138 h post-injection.
Showed a mean tumor uptake of 6.3%IA/mL at ~142.6 h post-injection via imaging.
Exhibited low normal organ uptake.
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Animal Model:CB17 SCID mice (female)[2]
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Dosage:522 kBq (4.7 μg) Zr-89 REGN2878 (biodistribution studies)
5.51 MBq (24 μg) Zr-89 REGN2878 (imaging studies) -
Administration:i.v.; single dose (biodistribution studies)
i.v.; single dose (imaging studies) -
Result:Reached a mean of 29.6%IA/g at 138 h post-injection.
Showed a mean tumor uptake of 34.0%IA/mL at ~143 h post-injection via imaging.
Exhibited low normal organ uptake.
Gene ID
Accession
Target
PRLR/Prolactin Receptor
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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Product Image
Application
ELISA, FACS, Functional assay
Chemical Information
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Appearance Liquid
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Color Colorless to light yellow
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Synonyms
PRLR ADC antibody
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Shipping
Shipping with dry ice.
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Patient-Derived Xenograft (PDX)
Patient-derived xenograft (PDX) models are generated by engrafting primary human tumor tissue directly into immunodeficient mice, allowing in vivo propagation of patient tumor biology without initial in vitro adaptation. These models are used to preserve key histopathological and molecular characteristics of the original tumor and enable assessment of tumor growth dynamics and therapeutic response in a living organism. The biological readout is tumor engraftment and subsequent growth in the murine host, which reflects the ability of human tumor cells to survive, vascularize, and expand in an immunocompromised microenvironment.
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Splenic/Portal-Vein Liver Metastasis Xenograft
Splenic and portal-vein liver metastasis xenograft models deliver tumor cells into the portal circulation so that cells reach the liver first and form hepatic metastatic lesions; splenic injection uses the spleen as an access route to the portal system, while direct portal-vein injection introduces cells into the portal vein without requiring splenectomy. The assay detects liver colonization, intrahepatic tumor growth, tumor distribution, treatment response, survival, and liver-metastasis microenvironment changes; readouts include bioluminescence or fluorescence imaging, gross liver nodule counts, liver weight or tumor burden, histology, and survival.
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Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
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Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
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Orthotopic Cell-Line Xenograft
Orthotopic cell-line xenograft models involve implantation of human cancer cell lines into the anatomically corresponding organ of immunodeficient mice to reproduce tumor growth within a native microenvironment, enabling more clinically relevant tumor behavior compared with subcutaneous models. These models are widely used because orthotopic placement better recapitulates tumor progression, including invasion and metastatic spread, which are often underrepresented in heterotopic implantation systems. Compared with conventional xenografts, orthotopic implantation is described as more technically complex but provides improved simulation of tumor-microenvironment interactions and metastatic behavior, making it particularly valuable for translational oncology research. Surgical orthotopic implantation approaches have been emphasized as enabling faithful reproduction of clinical cancer features, including metastasis and disease progression patterns that align with the tumor’s organ of origi
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Intraperitoneal/Peritoneal Dissemination Xenograft
Intraperitoneal (IP) or peritoneal dissemination xenograft models are based on the introduction of human cancer cells into the peritoneal cavity of immunodeficient mice, where they attach to peritoneal surfaces, form multicellular aggregates or spheroids, and progressively generate disseminated tumor nodules that mimic advanced peritoneal metastatic disease. These models are widely used to study ovarian cancer progression, tumor-microenvironment interactions, and intraperitoneal therapeutic responses, often incorporating bioluminescence or fluorescence imaging to longitudinally monitor tumor burden in vivo. The biological principle relies on the capacity of tumor cells such as SKOV3 or related ovarian carcinoma lines to survive in suspension, aggregate within ascites-like fluid, adhere to mesothelial surfaces, and invade peritoneal organs, thereby recapitulating human peritoneal carcinomatosis patterns observed in advanced disease.
Purity & Documentation
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Data Sheet (267 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Inhibitory Antibodies User Guide (603 KB)
References
[1]. Kelly MP, et al. Preclinical Activity of the Novel Anti-Prolactin Receptor (PRLR) Antibody-Drug Conjugate REGN2878-DM1 in PRLR-Positive Breast Cancers. Mol Cancer Ther. 2017;16(7):1299-1311. [Content Brief]
[2]. Cheal SM, et al. ImmunoPET Imaging of Endogenous and Transfected Prolactin Receptor Tumor Xenografts. Mol Pharm. 2018;15(6):2133-2141. [Content Brief]
[3]. Anderson MG, et al. ABBV-176, a PRLR antibody drug conjugate with a potent DNA-damaging PBD cytotoxin and enhanced activity with PARP inhibition. BMC Cancer. 2021;21(1):681. Published 2021 Jun 9. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)