BTK (Phospho-Tyr223) ELISA Kit

Name: BTK (Phospho-Tyr223) ELISA Kit
SKU: DEIA-XYA307
Rating: 5 (1 reviews)

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

COA

SDS

Datasheet

Summary

Sample

cultured cells

Species Reactivity

Human; Mouse; Rat

Detection Method

Indirect ELISA

Intended Use

The BTK (Phospho-Tyr223) Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor BTK protein phosphorylation and expression profile in cells. The kit can be used for measuring the relative amounts of phosphorylated BTK in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on BTK phosphorylation.

Contents of Kit

1. 96-Well Cell Culture Clear-Bottom Microplate: 2 plates
2. 10x TBS: 24 mL (10x)
3. Quenching Buffer: 24 mL (1x)
4. Blocking Buffer: 50 mL (1x)
5. 10x Wash Buffer: 50 mL (10x)
6. 100x Anti-BTK (Phospho-Tyr223) Antibody (Rabbit Polyclonal): 60 μL (100x), Red
7. 100x Anti-BTK Antibody (Rabbit Polyclonal): 60 μL (100x), Purple
8. 100x Anti-GAPDH Antibody (Mouse Monoclonal): 60 μL (100x), Green
9. HRP-Conjugated Anti-Rabbit IgG Antibody: 12 mL (1x), Glass
10. HRP-Conjugated Anti-Mouse IgG Antibody: 12 mL (1x), Glass
11. Primary Antibody Diluent: 12 mL (1x)
12. Ready-to-Use Substrate: 12 mL (1x), Brown
13. Stop Solution: 12 mL (1x)
14. Crystal Violet Solution: 12 mL (1x), Glass
15. SDS Solution: 24 mL (1x)
16. Adhesive Plate Seals: 4 seals

Storage

4°C/6 Months

Citations

Have you cited DEIA-XYA307 in a publication? Let us know and earn a reward for your research.

Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Changes in primary and secondary hemostasis in patients with CLL treated with venetoclax and ibrutinib

LEUKEMIA & LYMPHOMA

Authors: Svanberg, Rebecka; Ostrowski, Sisse Rye; Nasserinejad, Kazem; Kersting, Sabina; Dobber, Johan A.; Mattson, Mattias; Tran, Hoa T. T.; Levin, Mark-David; Mous, Rogier; Kater, Arnon P.; Niemann, Carsten U.

Abstract

Bleeding is a common adverse event following ibrutinib monotherapy. However, it remains unclear how hemostasis is affected by venetoclax in combination with ibrutinib. Here we investigated hemostasis in patients with chronic lymphocytic leukemia (CLL) at baseline, during ibrutinib monotherapy, and during venetoclax and ibrutinib combination therapy or venetoclax monotherapy. Primary hemostasis, assessed by Multiplate using adenosine diphosphate (ADP), arachidonic acid (AA), and thrombin receptor agonist peptide (TRAP-6), was impaired in all CLL patients at baseline, remained unchanged upon ibrutinib monotherapy, and improved significantly following venetoclax added to ibrutinib or as monotherapy. Secondary hemostasis assessed by thromboelastography (TEG) was normal and unchanged throughout treatment. The frequency of clinical bleeding events was the highest during ibrutinib monotherapy, in line with the demonstrated improved primary hemostasis upon addition of venetoclax, thus pointing toward a treatment option for CLL patients with increased bleeding risk.

Design and synthesis of novel 1-substituted 3-(6-phenoxypyridin-3-yl)-1H-pyrazolo[3,4-d]pyrimidin-4-amine analogs as selective BTK inhibitors for the treatment of mantle cell lymphoma

BIOORGANIC CHEMISTRY

Authors: Ran, Fansheng; Liu, Yang; Yu, Shengping; Guo, Kaiwen; Tang, Wendi; Chen, Xin; Zhao, Guisen

Abstract

Ibrutinib (IBN), a first-in-class BTK-inhibitor, was approved by the FDA for the treatment of mantle cell lymphoma (MCL). Although IBN shows excellent performance as an anti-lymphoma agent, it has some undesirable side effects due to its off-target activities. Our studies yielded a novel series of 3-(6-phenoxypyridin-3-yl)-4-amine-1H-pyrazolo [3,4-d]pyrimidine derivatives capable of potent inhibition of Bruton's tyrosine kinase (BTK). Notably, compound 13e explained potent BTK inhibitory activity and could completely inhibit the phosphorylation of BTK and PLC gamma 2 in Z138 cells at low micromolar concentration. Compared with IBN, compound 13e improved anti-proliferative activities 3-40 folds in MCL cell lines with IC50 values lower than 1 mu M. Low micromolar doses of 13e could induce strong cell apoptosis in Jeko-1 and Z138 cells. In addition, compound 13e showed greater BTK selectivity and higher stability in human liver microsomes than IBN and potential safety improvement for the treatment of MCL.