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Name:Acalabrutinib
| Chemical structure | Code NO. |
MT1094 |
 |
Name |
Acalabrutinib |
Synonym |
ACP-196; ACP196; ACP 196 | |
CAS NO. |
1420477-60-6 | |
Chemical Formula |
C26H23N7O2 | |
MW |
465.51 | |
Purity |
>98% | |
Solubility(R.T.: 25℃) |
10 mM in DMSO | |
Stability |
- 20℃, 2 years |
Availability and price
|
Size |
Price |
Availability |
|
100mg |
$350 |
In stock |
|
250mg |
$700 |
In stock |
|
1g |
$1250 |
In stock |
|
>1g |
Get quote |
Get quote |
|
We match the best price and quality on market! | ||
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Description
Acalabrutinib (ACP-196) is a second-generation, selective, irreversible inhibitor of BTK (Bruton's tyrosine kinase) that has improved pharmacologic features, including favorable plasma exposure, rapid oral absorption, a short half-life, and the absence of irreversible targeting to alternative kinases, such as EGFR,TEC, and ITK.
Target: BTK
Acalabrutinib (ACP-196) is a more selective, irreversible BTK inhibitor that is specifically designed to improve on the safety and efficacy of first-generation BTK inhibitors. Acalabrutinib shows dose dependent inhibition of B-cell receptor signaling in primary CLL cells. In kinase-inhibition assays, acalabrutinib was a more selective BTK inhibitor than ibrutinib. These biochemical findings are physiologically relevant, because acalabrutinib did not
inhibit EGFR, TEC, or ITK signaling. The findings provide structural, biochemical, and in vitro differentiation of acalabrutinib from ibrutinib. These data, combined with objective clinical responses in a study of naturally occurring canine B-cell lymphomas, provided justification for the clinical development of acalabrutinib for the treatment of CLL.
Target: BTK
Acalabrutinib (ACP-196) is a more selective, irreversible BTK inhibitor that is specifically designed to improve on the safety and efficacy of first-generation BTK inhibitors. Acalabrutinib shows dose dependent inhibition of B-cell receptor signaling in primary CLL cells. In kinase-inhibition assays, acalabrutinib was a more selective BTK inhibitor than ibrutinib. These biochemical findings are physiologically relevant, because acalabrutinib did not
inhibit EGFR, TEC, or ITK signaling. The findings provide structural, biochemical, and in vitro differentiation of acalabrutinib from ibrutinib. These data, combined with objective clinical responses in a study of naturally occurring canine B-cell lymphomas, provided justification for the clinical development of acalabrutinib for the treatment of CLL.
References
Attention
Sold for research purposes only; not for human use of any kind.
