THAL SNS 032 - CAS 2139287-33-3

THAL SNS 032 is a potent and selective CDK9 degrader PROTAC consisting of a CDK-binding SNS-032 ligand conjugated to a cereblon E3 ligase ligand thalidomide. THAL SNS 032 was showed to inhibit proliferation of leukemia cell lines.

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Molecular Formula
Molecular Weight


    • Specification
      • Purity
        Shelf Life
        2 years
        Store at -20°C
        IUPAC Name
        N-(5-(((5-(tert-butyl)oxazol-2-yl)methyl)thio)thiazol-2-yl)-1-(14-((2-(2,6-dioxopiperidin-3-yl)-1,3-dioxoisoindolin-4-yl)amino)-2-oxo-6,9,12-trioxa-3-azatetradecyl)piperidine-4-carboxamide; 1-Piperidineacetamide, 4-[[[5-[[[5-(1,1-dimethylethyl)-2-oxazolyl]methyl]thio]-2-thiazolyl]amino]carbonyl]-N-[2-[2-[2-[2-[[2-(2,6-dioxo-3-piperidinyl)-2,3-dihydro-1,3-dioxo-1H-isoindol-4-yl]amino]ethoxy]ethoxy]ethoxy]ethyl]-; SNS-THAL-032; Thal-SNS-032; THAL-SNS-032
    • Properties
      • Density
        1.40±0.1 g/cm3
        InChI Key
        Canonical SMILES
    • Reference Reading
      • 1. Pharmacological perturbation of CDK9 using selective CDK9 inhibition or degradation.
        Olson, C.M., Jiang, B., Erb, M.A., Liang, Y., Doctor, Z.M., Zhang, Z., Zhang, T., Kwiatkowski, N., Boukhali, M., Green, J.L. and Haas, W., 2018. Nature chemical biology, 14(2), pp.163-170.
        Cyclin-dependent kinase 9 (CDK9), an important regulator of transcriptional elongation, is a promising target for cancer therapy, particularly for cancers driven by transcriptional dysregulation. We characterized NVP-2, a selective ATP-competitive CDK9 inhibitor, and THAL-SNS-032, a selective CDK9 degrader consisting of a CDK-binding SNS-032 ligand linked to a thalidomide derivative that binds the E3 ubiquitin ligase Cereblon (CRBN). To our surprise, THAL-SNS-032 induced rapid degradation of CDK9 without affecting the levels of other SNS-032 targets. Moreover, the transcriptional changes elicited by THAL-SNS-032 were more like those caused by NVP-2 than those induced by SNS-032. Notably, compound washout did not significantly reduce levels of THAL-SNS-032-induced apoptosis, suggesting that CDK9 degradation had prolonged cytotoxic effects compared with CDK9 inhibition. Thus, our findings suggest that thalidomide conjugation represents a promising strategy for converting multi-targeted inhibitors into selective degraders and reveal that kinase degradation can induce distinct pharmacological effects compared with inhibition.
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