CAS |
1420477-60-6 |
Chinese Name |
阿可替尼 |
English Name |
Acalabrutinib |
Synonyms |
;ACP196.Acalabrutinib;Acalabrutinib(ACP196);ACP-196;Acalabrutinib;氨丙基嘧吡啶; |
Molecular Formula |
C26H23N7O2 |
Molecular Weight |
465.51 |
Solubility |
Soluble in DMSO |
Purity |
HPLC≥98% |
Appearance |
Light yellow to yellow Solid |
Storage |
Powder:2-8℃,2 years;Insolvent(Mother Liquid):-20℃,6 months;-80℃,1 year |
EC |
EINECS 814-272-0 |
MDL |
MFCD29472294 |
SMILES |
O=C(NC1=NC=CC=C1)C2=CC=C(C3=C4C(N)=NC=CN4C([C@H]5N(C(C#CC)=O)CCC5)=N3)C=C2 |
InChIKey |
WDENQIQQYWYTPO-IBGZPJMESA-N |
InChI |
InChI=1S/C26H23N7O2/c1-2-6-21(34)32-15-5-7-19(32)25-31-22(23-24(27)29-14-16-33(23)25)17-9-11-18(12-10-17)26(35)30-20-8-3-4-13-28-20/h3-4,8-14,16,19H,5,7,15H2,1H3,(H2,27,29)(H,28,30,35)/t19-/m0/s1 |
PubChem CID |
71226662 |
Target Point |
Btk |
Passage |
Protein Tyrosine Kinase/RTK;Angiogenesis |
Background |
It is a selective second-generation BTK inhibitor with good target specificity. |
Biological Activity |
Acalabrutinib (ACP-196) 是选择性的第二代BTK抑制剂,抑制B细胞表面原抗体信号通路的激活,IC50为3 nM。它具有很好的靶标特异性,对BTK的选择性比对其他TEC激酶家族成员如ITK、TXK、BMK和TEC的选择性高323-, 94-, 19-, 9-倍。对EGFR没有活性。[1-3] |
In Vitro |
在初级人源慢性淋巴细胞白血病细胞的体外信号检测中,Acalabrutinib抑制下游靶标ERK、IKB、AKT的酪氨酸磷酸化。在9种与BTK半胱氨酸所在位置一致的激酶中,Acalabrutinib对BTK的选择性高于对其他激酶。Acalabrutinib不抑制EGFR、ITK和TEC,对EGFR在Y1068和Y1173位点的磷酸化没有影响。相对于ibrutinib,Acalabrutinib具有更高的IC50值,并几乎对 ITK,EGFR,ERBB2,ERBB4,JAK3,BLK,FGR,FYN,HCK,LCK,LYN,SRC以及YES1的激酶活性没有抑制作用[1]。 |
In Vivo |
对小鼠进行ACP-196的口服处理,在CD19+脾细胞中抑制了anti-IgM诱导的CD86表达,此抑制作用为剂量依赖性,ED50为0.34 mg/kg。在处理后3h,ACP-196抑制了>90%的CD86表达水平[3]。 |
Animal Experiment |
Animal Models: 犬类; Dosages: 2.5,5,10 mg/kg.; Administration: 口服[2] |
Data Literature Source |
[1] Wu J,et al. J Hematol Oncol. 2016,9:21. [2] Heather L. Gardner,et al .Cancer Res. 2014,74(19 Supplement):1744. [3] Todd Covey,et al. Cancer Res. 2015,75 (15 Supplement):2596. |
Unit |
Bottle |
Specification |
5mg 10mM*1mL in DMSO 10mg |