Anti-Human CD80 Recombinant Antibody (Galiximab) (CAT#: TAB-215)

Recombinant monoclonal antibody to CD8. Galiximab is a monoclonal antibody designed for the treatment of B-cell lymphoma. As of September 2009, The drug is a chimeric antibody from Macaca irus and Homo sapiens.


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Inhib

Figure 1 Galiximab inhibits cell proliferation of B-NHL cell lines and sensitizes B-NHL cells to apoptosis by CDDP and TRAIL.

Figure 1 Galiximab inhibits cell proliferation of B-NHL cell lines and sensitizes B-NHL cells to apoptosis by CDDP and TRAIL.

A, surface expression of CD80 on B-NHL cell lines. The surface expression of CD80 was analyzed by flow cytometry. A, representative histogram is shown for the various B-NHL cell lines and an isotype control is shown. In addition, the mean fluorescence intensity (MFI) is represented in the table. B, sensitization to apoptosis. B-NHL cell lines were treated with galiximab (20 mg/mL) for 18 hours and followed by treatment with CDDP (5 mg/mL) or TRAIL (5 ng/mL) for an additional 18 hours and apoptosis was determined by activation of caspase-3 (left) as described. Ã, P < 0.05; ÃÃ, P < 0.01. Apoptosis was also determined by Annexin-V as described (right). C, galiximab-induced inhibition of Raji cell viability and cell recovery. The B-NHL cell line Raji was treated with various concentrations of galiximab and incubated for different time periods (6-24 hours), and cell viability was determined by trypan blue dye exclusion and total cell recovery was recorded. Raji cells that were not treated with galiximab represented 100% viability. The data represent the mean AE SD from 3 independent experiments Ã, P < 0.05. D, galiximab sensitizes resistant B-NHL cell lines to apoptosis by CDDP and TRAIL. Sensitization of B-NHL Raji cells by galiximab to apoptosis by CDDP or TRAIL is synergistic. Raji cells were treated with various concentrations of galiximab (10-100 mg/mL) for 18 hours and then treated with either CDDP (5, 10, and 20 mg/mL; left) or only one concentration of galiximab (20 mg/mL) and various concentrations of TRAIL (2.5, 5, and 10 ng/mL; right) for an additional 18 hours and apoptosis was determined. The data represent the mean AE SD from 3 independent experiments. Ã, P < 0.05; ÃÃ, P < 0.01. In addition, the data were analyzed for synergy by isobologram analysis as described in Materials and Methods. The isobologram is represented left of D. AAD, aminoactinomycin D.

Martinez-Paniagua, M. A., Vega, M. I., Huerta-Yepez, S., Baritaki, S., Vega, G. G., Hariharan, K., & Bonavida, B. (2012). Galiximab Signals B-NHL Cells and Inhibits the Activities of NF-κB–Induced YY1-and Snail-Resistant Factors: Mechanism of Sensitization to Apoptosis by Chemoimmunotherapeutic Drugs. Molecular cancer therapeutics, 11(3), 572-581.

WB

Figure 2 Galiximab inhibits NF-kB activity in Raji cells and the role of NF-kB inhibition in the sensitization of Raji to apoptosis by CDDP and TRAIL.

Figure 2 Galiximab inhibits NF-kB activity in Raji cells and the role of NF-kB inhibition in the sensitization of Raji to apoptosis by CDDP and TRAIL.

Raji cells were treated with different concentrations of galiximab (25, 50, and 100 mg/mL) for 18 hours, and aliquots were used to prepare both nuclear and total cell lysates as described in Materials and Methods. A, Western blot analysis for NF-kB expression. Total cell lysates were tested for various gene products of the NF-kB pathway. b-Actin was used as a loading control. Densitometric analysis is also shown and intensity of the bands was normalized to b-actin bands. B, inhibition of NF-kB DNA-binding activity by galiximab. Raji cells were treated with galiximab (25 mg/mL). Nuclear lysates were tested for NF-kB DNAbinding activity by EMSA as described. The NF-kB inhibitor DHMEQ (10 mg/mL) was used as a positive control and cold probes as competitors. For the supershift assay, the nuclear proteins were incubated with anti-p65 antibody overnight at 4 C before the analysis by EMSA. C, galiximab-induced inhibition of NF-kB in the sensitization to apoptosis by CDDP and TRAIL. Raji cells were treated with galiximab (20 mg/mL) for 18 hours or with the NF-kB inhibitor DHMEQ (10 mg/mL) for 18 hours and the cells were subsequently treated with either CDDP (5 mg/mL) or TRAIL (5 mg/mL) for an additional 24 hours and apoptosis was determined. The data represent the mean AE SD from 3 independent experiments. Ã, P < 0.01. D, inhibition of the AKT pathway by galiximab. Total cell lysates were tested for various gene products of the AKT pathway. b-Actin was used as a loading control. Densitometric analysis is also shown.

Martinez-Paniagua, M. A., Vega, M. I., Huerta-Yepez, S., Baritaki, S., Vega, G. G., Hariharan, K., & Bonavida, B. (2012). Galiximab Signals B-NHL Cells and Inhibits the Activities of NF-κB–Induced YY1-and Snail-Resistant Factors: Mechanism of Sensitization to Apoptosis by Chemoimmunotherapeutic Drugs. Molecular cancer therapeutics, 11(3), 572-581.

WB

Figure 3 Galiximab inhibits the expression and the activity of the transcription factors YY1 and Snail in Raji cells.

Figure 3 Galiximab inhibits the expression and the activity of the transcription factors YY1 and Snail in Raji cells.

Inhibition of YY1 and Snail by galiximab. Raji cells were treated with various concentrations of galiximab (25, 50, and 100 mg/mL) for 18 hours and total cell lysates were prepared for Western blot analysis. b-Actin was used as a loading control. The Western blots analyses were also analyzed by densitometry and is shown below the Western blot analysis figure.

Martinez-Paniagua, M. A., Vega, M. I., Huerta-Yepez, S., Baritaki, S., Vega, G. G., Hariharan, K., & Bonavida, B. (2012). Galiximab Signals B-NHL Cells and Inhibits the Activities of NF-κB–Induced YY1-and Snail-Resistant Factors: Mechanism of Sensitization to Apoptosis by Chemoimmunotherapeutic Drugs. Molecular cancer therapeutics, 11(3), 572-581.

FC

Figure 4 Galiximab inhibits cell proliferation of B-NHL cell lines and sensitizes B-NHL cells to apoptosis by CDDP and TRAIL.

Figure 4 Galiximab inhibits cell proliferation of B-NHL cell lines and sensitizes B-NHL cells to apoptosis by CDDP and TRAIL.

A, surface expression of CD80 on B-NHL cell lines. The surface expression of CD80 was analyzed by flow cytometry. A, representative histogram is shown for the various B-NHL cell lines and an isotype control is shown. In addition, the mean fluorescence intensity (MFI) is represented in the table. B, sensitization to apoptosis. B-NHL cell lines were treated with galiximab (20 μg/mL) for 18 hours and followed by treatment with CDDP (5 μg/mL) or TRAIL (5 ng/mL) for an additional 18 hours and apoptosis was determined by activation of caspase-3 (left) as described. *, P < 0.05; **, P < 0.01. Apoptosis was also determined by Annexin-V as described (right). C, galiximab-induced inhibition of Raji cell viability and cell recovery. The B-NHL cell line Raji was treated with various concentrations of galiximab and incubated for different time periods (6–24 hours), and cell viability was determined by trypan blue dye exclusion and total cell recovery was recorded. Raji cells that were not treated with galiximab represented 100% viability. The data represent the mean ± SD from 3 independent experiments *, P < 0.05. D, galiximab sensitizes resistant B-NHL cell lines to apoptosis by CDDP and TRAIL. Sensitization of B-NHL Raji cells by galiximab to apoptosis by CDDP or TRAIL is synergistic. Raji cells were treated with various concentrations of galiximab (10–100 μg/mL) for 18 hours and then treated with either CDDP (5, 10, and 20 μg/mL; left) or only one concentration of galiximab (20 μg/mL) and various concentrations of TRAIL (2.5, 5, and 10 ng/mL; right) for an additional 18 hours and apoptosis was determined. The data represent the mean ± SD from 3 independent experiments. *, P < 0.05; **, P < 0.01. In addition, the data were analyzed for synergy by isobologram analysis as described in Materials and Methods. The isobologram is represented left of D. AAD, aminoactinomycin D.

Martinez-Paniagua, M. A., Vega, M. I., Huerta-Yepez, S., Baritaki, S., Vega, G. G., Hariharan, K., & Bonavida, B. (2012). Galiximab Signals B-NHL Cells and Inhibits the Activities of NF-κB–Induced YY1-and Snail-Resistant Factors: Mechanism of Sensitization to Apoptosis by Chemoimmunotherapeutic Drugs. Molecular cancer therapeutics, 11(3), 572-581.

Activ

Figure 5 Galiximab inhibits the expression and the activity of the transcription factors YY1 and Snail in Raji cells.

Figure 5 Galiximab inhibits the expression and the activity of the transcription factors YY1 and Snail in Raji cells.

A, inhibition of YY1 and Snail by galiximab. Raji cells were treated with various concentrations of galiximab (25, 50, and 100 μg/mL) for 18 hours and total cell lysates were prepared for Western blot analysis. β-Actin was used as a loading control. The Western blots analyses were also analyzed by densitometry and is shown below the Western blot analysis figure. B, galiximab inhibits the DNA-binding activity of YY1 and Snail. Raji cells were treated with galiximab (25 μg/mL) for 18 hours and nuclear lysates were tested for DNA-binding activities for YY1 and Snail as described in Materials and Methods. The specificity of DNA-binding activity was determined by the use of a corresponding competitive cold probe and in the absence of nuclear extracts in the assay.

Martinez-Paniagua, M. A., Vega, M. I., Huerta-Yepez, S., Baritaki, S., Vega, G. G., Hariharan, K., & Bonavida, B. (2012). Galiximab Signals B-NHL Cells and Inhibits the Activities of NF-κB–Induced YY1-and Snail-Resistant Factors: Mechanism of Sensitization to Apoptosis by Chemoimmunotherapeutic Drugs. Molecular cancer therapeutics, 11(3), 572-581.


Specifications

  • Immunogen
  • CD80-transfected CHO cell line.
  • Host Species
  • primate
  • Derivation
  • Chimeric (primate/human)
  • Type
  • IgG1 - lambda
  • Specificity
  • Tested positive against native human antigen.
  • Species Reactivity
  • Human
  • Applications
  • WB, ELISA, FC, IP, FuncS, IF, Neut, Inhib, Activ
  • CAS
  • 357613-77-5
  • Generic Name
  • Galiximab
  • UNII
  • S9OX9692ZB
  • Related Disease
  • Non-Hodgkin's lymphoma (NHL)

Product Property

  • Purity
  • >95.0%, determined by analysis by RP-HPLC & analysis by SDS-PAGE.
  • Storage
  • Store at 4°C for up to 3 months. For longer term storage aliquot into small volumes and store at -20°C.

Applications

  • Application Notes
  • The CD80 antibody has been reported in applications of WB, ELISA, FC, IP, FuncS, IF, Neut, Inhib, Activ.

Target

  • Alternative Names
  • Galiximab;357613-77-5;IDEC-114;16C10;CD80;CD80 molecule;CD28LG, CD28LG1, CD80 antigen (CD28 antigen ligand 1, B7 1 antigen) , CD80 molecule;T-lymphocyte activation antigen CD80;B lymphocyte activation antigen B7;B7 1;B7.1;activation B7-1 antigen;costimula

Related Resources

  • Related Diseases

Product Notes

This is a product of Creative Biolabs' Hi-Affi™ recombinant antibody portfolio, which has several benefits including:

• Increased sensitivity
• Confirmed specificity
• High repeatability
• Excellent batch-to-batch consistency
• Sustainable supply
• Animal-free production

See more details about Hi-Affi™ recombinant antibody benefits.

Downloads

Download resources about recombinant antibody development and antibody engineering to boost your research.

See other products for "Galiximab"

Afuco™ Anti-CD80 ADCC Recombinant Antibody (Galiximab), ADCC Enhanced
This product is an ADCC enhanced antibody produced by our Afuco™ platform. Recombinant monoclonal antibody to CD8. Galiximab is a monoclonal antibody designed for the treatment of B-cell lymphoma. As of September 2009, The drug is a chimeric antibody from Macaca irus and Homo sapiens.

See other products for "CD80"

Immunotoxin

CAT Product Name Application Type
AGTO-L001G anti-CD80 immunotoxin 6G7 (IgG)-Gel Cytotoxicity assay, Functional assay
AGTO-L001S anti-CD80 immunotoxin 6G7 (IgG)-Sap Cytotoxicity assay, Functional assay
AGTO-L001O anti-CD80 immunotoxin 6G7 (IgG)-Bouganin Cytotoxicity assay, Functional assay

Fc Glycosylation

CAT Product Name Application Type
Gly-159LC Recombinant Anti-Human CD80 Antibody (Fc glycosylation/Non fucosylated) ELISA Chimeric antibody (primate/human)

Low- or Non-fucosylated Oligosaccharide

CAT Product Name Application Type
Gly-159LC-1 Recombinant Anti-Human CD80 Antibody (Fc glycosylation/Non fucosylated) ELISA Chimeric antibody (primate/human)

Chicken IgY Antibody

CAT Product Name Application Type
BRD-0066MZ Chicken Anti-BB1 Polyclonal IgY WB Chicken antibody

Neutralizing Antibody

Blocking Antibody

Rabbit Monoclonal Antibody

CAT Product Name Application Type
MOR-0583 Hi-Affi™ Rabbit Anti-CD80 Recombinant Antibody (clone DS583AB) WB, IHC Rabbit IgG

ADCC Enhanced Antibody

CAT Product Name Application Type
AFC-TAB-215 Afuco™ Anti-CD80 ADCC Recombinant Antibody (Galiximab), ADCC Enhanced ELISA, FC, IP, FuncS, IF ADCC enhanced antibody

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For research use only. Not intended for any clinical use. No products from Creative Biolabs may be resold, modified for resale or used to manufacture commercial products without prior written approval from Creative Biolabs.

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