2. Vitamin D Related/Nuclear Receptor Stem Cell/Wnt JAK/STAT Signaling PI3K/Akt/mTOR
  3. Estrogen Receptor/ERR STAT Akt
  4. XOMA-213

XOMA-213  (Synonyms: LFA-102; X213)

Cat. No.: HY-P991358 Pureza: 98.46%
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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.

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XOMA-213

XOMA-213 Estructura química

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XOMA-213 Related Antibodies

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Descripciòn

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[1].

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.

XOMA-213 Related Antibodies

Western Blot Analysis[1]

Cell Line: T47D human ER+ breast cancer cells, MCF7 human ER+ breast cancer cells, dissociated primary human breast tumor cells (ER+/PR+/HER2-)
Concentration: 0.05, 0.1, 0.5, 1, 5 μg/mL (T47D/MCF7 cells); 10 μg/mL (primary tumor cells); 50 ng/mL hPRL
Incubation Time: 30 min (pre-incubation at 37°C); 30 min (hPRL stimulation)
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.

Cell Proliferation Assay[1]

Cell Line: T47D human ER+ breast cancer cells, Nb2-11 rat pre-T cell lymphoma cells, BaF3/hPRLR cells, BaF3/hPRLR/hPRL cells
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
Incubation Time: 96 h (T47D cells); 96 h (BaF3/hPRLR cells with hPRL); 168 h (BaF3/hPRLR/hPRL cells)
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

LFA102 (10 mg/kg; i.v.; single dose) completely blocks prolactin receptor signaling in T47D-T2 human breast cancer xenografts in female SCID mice[1].
LFA102 (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].
LFA102 (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].
LFA102 (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.

Animal Model: SCID mice (female)[1]
Dosage: 10 mg/kg
Administration: i.v.; single dose
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.
Animal Model: SCID mice (female)[1]
Dosage: 0.01-10 mg/kg
Administration: i.p.; single dose
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.
Animal Model: rats (female; DMBA-induced mammary tumor model)[1]
Dosage: 300 mg/kg (monotherapy); 300 mg/kg (combination therapy)
Administration: i.p.; twice weekly (monotherapy); three times weekly (combination therapy)
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.
Animal Model: rats (ovariectomized female)[1]
Dosage: 50 mg/kg
Administration: i.p.; daily; 5 days
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
Gene ID

5618  [NCBI]

Accession
Application

ELISA, FACS, Functional assay
Conjugated

Unconjugated
Reconsititution

The product can be reconstituted/diluted with sterile PBS or saline.
Peso molecular

147.29 kDa

Appearance

Liquid

Color

Colorless to light yellow

SMILES

[XOMA-213]
Envío

Shipping with dry ice.
Formulation

Please refer to the lot-specific COA for specific buffer information.
Almacenamiento

Please store the product under the recommended conditions in the Certificate of Analysis.
Pureza y Documentación
Referencias
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XOMA-213 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

XOMA-213LFA-102 X213XOMA213XOMA 213LFA102LFA 102X213X 213X-213Estrogen Receptor/ERRSTATAktPKBProtein kinase BNb2-11 cellsPRLRPRLT47D cellsMCF7 cellsprolactinhuman growth hormoneprolactin receptorbreast cancerhGHInhibitorinhibitorinhibit

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