BTX161 |
Katalog-Nr.GC62880 |
BTX161, ein Thalidomid-Analogon, ist ein potenter CKIα-Abbauer. BTX161 vermittelt den Abbau von CKIα in menschlichen AML-Zellen besser als Lenalidomid und aktiviert DNA Damage Response (DDR) und p53, wÄhrend es den p53-Antagonisten MDM2 stabilisiert.
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Cas No.: 2052301-24-1
Sample solution is provided at 25 µL, 10mM.
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].
[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.
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