| Company Name: |
BOC Sciences |
| Tel: |
16314854226; +8616314854226 |
| Email: |
inquiry@bocsci.com |
BTX161 manufacturers
- BTX161
-
- $1490.00
-
2026-04-20
- CAS:2052301-24-1
- Purity:
- Supply Ability: 10g
|
| Product Name: | BTX161 | | Synonyms: | BTX161;1H-Azepine-2,7-dione, 3-(1,3-dihydro-4-methyl-1-oxo-2H-isoindol-2-yl)tetrahydro-, (3S)-;(S)-3-(4-Methyl-1-oxoisoindolin-2-yl)azepane-2,7-dione | | CAS: | 2052301-24-1 | | MF: | C15H16N2O3 | | MW: | 272.3 | | EINECS: | | | Product Categories: | | | Mol File: | 2052301-24-1.mol |  |
| | BTX161 Chemical Properties |
| Boiling point | 558.7±50.0 °C(Predicted) | | density | 1.301±0.06 g/cm3(Predicted) | | storage temp. | Store at -20°C | | form | Solid | | pka | 10.83±0.40(Predicted) | | color | White to off-white |
| | BTX161 Usage And Synthesis |
| Uses | BTX161, a thalidomide analog, is an effective CKIα degrader. BTX161 mediates human AML cell CKIα degradation more effectively than lenalidomide and activates the DNA damage response (DDR) and p53, while stabilizing p53 antagonist MDM2. | | Biological Activity | BTX161, a Thalidomide analog, is a potent CKIα degrader. BTX161 mediates degradation of CKIα better than Lenalidomide in human AML cells and activates DNA damage response (DDR) and p53, while stabilizing the p53 antagonist MDM2[1].
BTX161 (25 μM; 4 hours; MV4-11 cells) upregulates all the Wnt targets including MYC and did not affect MDM2 mRNA expression[1].BTX161 (10 μM; 6 hours; MV4-11 cells), on its own, augmented p53 and MDM2 protein expression, yet in combination with THZ1, and particularly with both THZ1 and CDK9, further augmented p53 and induced maximal caspase 3 activation[1]. | | References | [1]. Minzel W, et al. Small Molecules Co-targeting CKIα and the Transcriptional Kinases CDK7/9 Control AML in Preclinical Models. Cell. 2018;175(1):171-185.e25. |
| | BTX161 Preparation Products And Raw materials |
|