XOMA-213
Based on 1 Customer Validation
XOMA-213 (LFA-102; X213) is a human monoclonal antibody (mAb) targeting the prolactin receptor (PRLR), with a Kd value of 2 nM against the human target. XOMA-213 blocks PRL-induced cell proliferation and inhibits the activation of multiple PRLR ligands, including PRL and human growth hormone (hGH). XOMA-213 suppresses PRL-induced phosphorylation of Stat5, Akt and ERK1/2 in cells. XOMA-213 induces tumor regression, delays disease progression, and inhibits PRLR signaling as well as tumor growth. XOMA-213 can be used in research related to breast cancer.
Para uso exclusivo en investigación. No vendemos a pacientes.
- Pureza: 98.46%
- Peso molecular:147.29 kDa
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Almacenamiento:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Actividad biológica
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Chemical Information
- Pureza y Documentación
- Referencias
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Help & FAQs
Actividad biológica
Descripciòn
Isotype
Human IgG1 kappa
Recommend Isotype Controls
Species Reactivity
Human
IC50 & Target
[1]|
STAT5 |
In Vitro
XOMA-213 (10 μg/mL) specifically binds to endogenous human and rat PRLR expressed on the surface of T47D, MCF7, Nb2-11, BaF3/hPRLR cells and primary human breast tumor cells, but does not bind to mouse PRLR or PRLR-negative BaF3 cells[1].
XOMA-213 (0.01-10 μg/mL; pre-incubated on ice for 45 min) binds to T47D cells without interfering with the PRL-PRLR interaction, exhibiting a non-ligand competitive binding mode[1].
XOMA-213 (0.05-10 μg/mL; 30 min pre-incubation at 37°C) potently inhibits hPRL-induced phosphorylation of Stat5, Akt and ERK1/2 in T47D cells, suppresses hPRL-induced Stat5 phosphorylation in MCF7 cells, and completely blocks hPRL-induced Stat5 phosphorylation in ER+/PR+/HER2- primary human breast tumor cells, with no detectable agonist activity[1].
XOMA-213 (0.01-100 μg/mL; 96-168 h) completely blocks hPRL-induced proliferation of T47D cells, potently inhibits the survival of Nb2-11 cells, suppresses hPRL- and hGH-induced proliferation in BaF3/hPRLR cells (EC50 = 0.5 μg/mL), and inhibits autocrine PRL-dependent growth in BaF3/hPRLR/hPRL cells. It performs better than ligand-competitive antagonists in high-ligand environments[1].
XOMA-213 (0.001-100 μg/mL; 24 h) induces antibody-dependent cell-mediated cytotoxicity (ADCC) against T47D cells, with a maximum cell killing rate of 50% and an EC50 of 0.13 μg/mL, demonstrating an additional antitumor mechanism of action[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:T47D human ER+ breast cancer cells, MCF7 human ER+ breast cancer cells, dissociated primary human breast tumor cells (ER+/PR+/HER2-)
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Concentration:0.05, 0.1, 0.5, 1, 5 μg/mL (T47D/MCF7 cells); 10 μg/mL (primary tumor cells); 50 ng/mL hPRL
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Incubation Time:30 min (pre-incubation at 37°C); 30 min (hPRL stimulation)
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Result:Neutralized hPRL-induced phosphorylation of Stat5, Akt, and ERK1/2 in a concentration-dependent manner in T47D cells.
Antagonized hPRL-induced Stat5 phosphorylation efficiently in MCF7 cells.
Completely neutralized hPRL-induced Stat5 phosphorylation in primary human breast tumor cells at 10 μg/mL.
Did not induce PRLR signaling in any cell type alone.
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Cell Line:T47D human ER+ breast cancer cells, Nb2-11 rat pre-T cell lymphoma cells, BaF3/hPRLR cells, BaF3/hPRLR/hPRL cells
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Concentration:10 μg/mL (T47D cells); 0.01-10 μg/mL (Nb2-11 cells); 0.01-10 μg/mL, 10 μg/mL (BaF3/hPRLR cells with hPRL); 0.03-3 μg/mL (BaF3/hPRLR cells with hGH); 0.01-100 μg/mL (BaF3/hPRLR/hPRL cells); 10-2000 ng/mL hPRL; 50 ng/mL hPRL; 1-100 ng/mL hPRL; 50 ng/mL hGH
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Incubation Time:96 h (T47D cells); 96 h (BaF3/hPRLR cells with hPRL); 168 h (BaF3/hPRLR/hPRL cells)
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Result:Completely neutralized hPRL-induced proliferation of T47D cells at physiological and super-physiological hPRL concentrations.
Completely inhibited Nb2-11 cell survival.
Inhibited hPRL-dependent growth of BaF3/hPRLR cells with an EC50 of 0.5 μg/mL, efficiently neutralized signaling even at high hPRL concentrations, and potently blocked hGH-induced proliferation.
Suppressed baseline autocrine Stat5 signaling and inhibited growth of BaF3/hPRLR/hPRL cells, while other PRLR antagonists did not.
In Vivo
XOMA-213 (0.01-10 mg/kg; i.p.; single dose) induces regression of Nb2-11-luc lymphoma xenografts and significantly prolongs time to progression in female SCID mice[1].
XOMA-213 (300 mg/kg; i.p.) inhibits growth and induces regression of DMBA-induced rat mammary tumors, and enhances the efficacy of letrozole when administered in combination[1].
XOMA-213 (50 mg/kg; i.p.; daily; 5 days) significantly elevates serum PRL levels in ovariectomized female rats, indicating effective systemic prolactin receptor neutralization[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:SCID mice (female)[1]
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Dosage:10 mg/kg
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Administration:i.v.; single dose
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Result:Completely blocked ovine PRL-induced intra-tumoral phosphorylated Stat5 (p-Stat5) levels, with no detectable p-Stat5 observed in treated tumors.
Reached serum levels ranging from 30-56 μg/mL at sample collection.
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Animal Model:SCID mice (female)[1]
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Dosage:0.01-10 mg/kg
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Administration:i.p.; single dose
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Result:Induced disease regression by day 3 post-dosing at ≥0.3 mg/kg, with efficacy sustained through day 14 post-dosing relative to controls.
Reduced mean photon count to 5.6 × 105 photons/second in the 10 mg/kg group on day 14, compared to 1.7 × 109 photons/second for controls.
Significantly prolonged time to progression for groups receiving ≥0.3 mg/kg relative to controls.
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Animal Model:rats (female; DMBA-induced mammary tumor model)[1]
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Dosage:300 mg/kg (monotherapy); 300 mg/kg (combination therapy)
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Administration:i.p.; twice weekly (monotherapy); three times weekly (combination therapy)
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Result:Exhibited significant anti-tumor activity from study days 10 through 27 post-dosing as monotherapy, with 33% of tumors regressing compared to 11% spontaneous regression in controls.
Showed significant efficacy relative to vehicle from days 9-20 post-dosing as monotherapy or combined with letrozole; combination had higher activity than letrozole alone from days 6-16 post-dosing.
Achieved 20% tumor regression with monotherapy and 47% with combination on day 20, compared to 0% with letrozole alone or vehicle.
Resulted in mean tumor volume of 809 mm3 with monotherapy and 436 mm3 with combination on day 20, compared to 1964 mm3 for vehicle.
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Animal Model:rats (ovariectomized female)[1]
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Dosage:50 mg/kg
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Administration:i.p.; daily; 5 days
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Result:Significantly elevated mean serum rat PRL levels on days 1-7 relative to controls, with a positive correlation between serum LFA102 levels and elevated PRL.
Ensayo clínico
| NCT Number | Sponsor | Condition | Start Date |
Phase
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Gene ID
Accession
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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Product Image
Aplicación
ELISA, FACS, Functional assay
Chemical Information
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Appearance Liquid
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Peso molecular 147.29 kDa
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Color Colorless to light yellow
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SMILES
[XOMA-213]
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Synonyms
LFA-102; X213
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Envío
Shipping with dry ice.
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureza y Documentación
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Ficha de datos (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)
Referencias
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
XOMA-213 Related Classifications
HY-P991358 Related Classifications
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