Human ErbB3 ELISA kit (DEIA5343)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
serum, plasma, cell culture supernatant, urine
Species Reactivity
Human
Intended Use
The Human ErbB3 (Epidermal Factor Growth Factor Receptor 3) ELISA (Enzyme-Linked Immunosorbent Assay) kit is an in vitro enzyme-linked immunosorbent assay for the quantitative measurement of human ErbB3 in serum, plasma, cell culture supernatants and urine.
Contents of Kit
1. ErbB3 Microplate: 96 wells (12 strips x 8 wells) coated with anti-human ErbB3.
2. Wash Buffer Concentrate (20X): 25 mL of 20X concentrated solution.
3. Standards: 2 vials of recombinant human ErbB3.
4. Assay Diluent A: 30 mL diluent buffer, 0.09% sodium azide as preservative. For Standard/Sample (serum/plasma) diluent.
5. Assay Diluent B: 15 mL of 5X concentrated buffer. For Standard/Sample (cell culture medium/urine) diluent.
6. Detection Antibody ErbB3: 2 vial of biotinylated anti-human ErbB3.
7. HRP-Streptavidin Concentrate: 200 μL 200X concentrated HRP-conjugated streptavidin.
8. TMB One-Step Substrate Reagent: 12 mL of 3, 3', 5, 5'-tetramethylbenzidine (TMB) in buffer solution.
9. Stop Solution: 8 mL of 0.2 M sulfuric acid.
Storage
May be stored for up to 6 months at 2-8°C from the date of shipment. Standard (recombinant protein) should be stored at -20°C or -80°C (recommended at -80°C) after reconstitution. Opened Microplate Wells or reagents may be stored for up to 1 month at 2-8°C. Return unused wells to the pouch containing desiccant pack, reseal along entire edge.
Note: the kit can be used within one year if the whole kit is stored at -20°C. Avoid repeated freeze-thaw cycles.
Precision
Intra-assay: CV<10%
Inter-assay: CV<12%
Sensitivity
4 pg/mL

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References


Paired genetic analysis by next-generation sequencing of lung cancer and associated idiopathic pulmonary fibrosis

CANCER SCIENCE

Authors: Otsubo, Kohei; Iwama, Eiji; Ijichi, Kayo; Kubo, Naoki; Yoneshima, Yasuto; Inoue, Hiroyuki; Tanaka, Kentaro; Osoegawa, Atsushi; Tagawa, Tetsuzo; Nakanishi, Yoichi; Okamoto, Isamu

The pathogenesis of lung cancer associated with idiopathic pulmonary fibrosis (IPF) has remained largely uncharacterized. To provide insight into this condition, we undertook genomic profiling of IPF-associated lung cancer as well as of adjacent fibrosing lung tissue in surgical specimens. Isolated DNA and RNA from 17 IPF-associated non-small cell lung cancer and 15 paired fibrosing lung tissue specimens were analyzed by next-generation sequencing with a panel that targets 161 cancer-related genes. Somatic genetic alterations were frequently identified in TP53 (n = 6, 35.3%) and PIK3CA (n = 5, 29.4%) genes in tumor samples as well as in EGFR (n = 7, 46.7%), PIK3CA (n = 5, 33.3%), ERBB3 (n = 4, 26.7%), and KDR (n = 4, 26.7%) in IPF samples. Genes related to the RAS-RAF signaling pathway were also frequently altered in tumor (n = 7, 41.2%) and IPF (n = 3, 20.0%) samples. The number of somatic alterations identified in IPF samples was almost as large as that detected in paired tumor samples (81 vs 90, respectively). However, only 6 of the 81 somatic alterations detected in IPF samples overlapped with those in paired tumor samples. The accumulation of somatic mutations was thus apparent in IPF tissue of patients with IPF-associated lung cancer, and the RAS-RAF pathway was implicated in lung tumorigenesis. The finding that somatic alterations were not frequently shared between tumor and corresponding IPF tissue indicates that IPF-associated lung cancer does not develop through the stepwise accumulation of somatic alterations in IPF.

Phase II Study of the Dual EGFR/HER3 Inhibitor Duligotuzumab (MEHD7945A) versus Cetuximab in Combination with FOLFIRI in Second-Line RAS Wild-Type Metastatic Colorectal Cancer

CLINICAL CANCER RESEARCH

Authors: Hill, Andrew G.; Findlay, Michael P.; Burge, Matthew E.; Jackson, Christopher; Alfonso, Pilar Garcia; Samuel, Leslie; Ganju, Vinod; Karthaus, Meinolf; Amatu, Alessio; Jeffery, Mark; Di Bartolomeo, Maria; Bridgewater, John; Coveler, Andrew L.; Hidalgo, Manuel; Kapp, Amy V.; Sufan, Roxana I.; McCall, Bruce B.; Hanley, William D.; Penuel, Elicia M.; Pirzkall, Andrea; Tabernero, Josep

Purpose: Duligotuzumab is a dual-action antibody directed against EGFR and HER3. Experimental Design: Metastatic colorectal cancer (mCRC) patients with KRAS ex2 wild-type received duligotuzumab or cetuximab and FOLFIRI until progression or intolerable toxicity. Mandatory tumor samples underwent mutation and biomarker analysis. Efficacy analysis was conducted in patients with RAS exon 2/3 wild-type tumors. Results: Of 134 randomly assigned patients, 98 had RAS ex2/3 wild-type. Duligotuzumab provided no progression-free survival (PUS) or overall survival (OS) benefit compared with cetuximab, although there was a trend for a lower objective response rate (ORR) in the duligotuzumab arm. No relationship was seen between HS or ORR and ERBB3, NRC1, or AREC expression. it were fewer skin rash events for duligotuzumab but more diarrhea. Although the incidence of grade >= 3 AEs was similar, the frequency of serious ALs was higher for duligotuzumab. Conclusions: Duligotuzumab plus FOLFIRI did not appear to improve the outcomes in patients with RAS exon 2/3 wild-type mCRC compared with cetuximab + FOLHRI. (C) 2018 AACR.

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