2052301-24-1
Chemical Structure
BTX161
- CAS No.: 2052301-24-1
- Formula:C15H16N2O3
- Molecular Weight:272.30
IUPAC Name: (S)-3-(4-methyl-1-oxoisoindolin-2-yl)azepane-2,7-dione
InChIKey: CNIZBMYCKRUTHY-LBPRGKRZSA-N
SMILES: O=C([C@@H](N(CC1=C2C=CC=C1C)C2=O)CCC3)NC3=O
Biological Activity: BTX161, a Thalidomide (HY-14658) analog, is a molecular glue degrader targeting CK1α. BTX161 recruits CK1α and the CK1α-FAM83 complex to the Cul4ACRBN E3 ligase complex, thereby driving ubiquitination and proteasomal degradation. BTX161 reduces FAM83G abundance through CK1α-FAM83G co-stability, slightly decreases FAM83H levels, but has no effect on the expression of FAM83B. BTX161 activates DNA damage response (DDR) and upregulates Wnt target genes including MYC. BTX161 can be used in research related to colorectal cancer, type b myelomonocytic leukemia and acute myeloid leukemia[1][2][3].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
|
BTX161 | 99.20% | BTX161, a Thalidomide (HY-14658) analog, is a molecular glue degrader targeting CK1α. BTX161 recruits CK1α and the CK1α-FAM83 complex to the Cul4ACRBN E3 ligase complex, thereby driving ubiquitination and proteasomal degradation. BTX161 reduces FAM83G abundance through CK1α-FAM83G co-stability, slightly decreases FAM83H levels, but has no effect on the expression of FAM83B. BTX161 activates DNA damage response (DDR) and upregulates Wnt target genes including MYC. BTX161 can be used in research related to colorectal cancer, type b myelomonocytic leukemia and acute myeloid leukemia. | ||||||||||||||||||||
|
loading...
/
|
|||||||||||||||||||||||
References
- [1]. Dunbar K, et al. IMiDs induce FAM83F degradation via an interaction with CK1α to attenuate Wnt signalling. Life science alliance. 2021 Feb;4(2):e202000804.
- [2]. Glennie L, et al. The Contribution of Native Protein Complexes to Targeted Protein Degradation. ACS Chem Biol. 2026 May 15;21(5):1095-1111.
- [3]. Minzel W, et al. Small Molecules Co-targeting CKIα and the Transcriptional Kinases CDK7/9 Control AML in Preclinical Models. Cell. 2018 Sep 20;175(1):171-185.e25. [Content Brief]
