THAL SNS 032
PROTAC comprising the cyclin-dependent kinase inhibitor SNS 032 (Cat. No. 4075) conjugated to the cereblon E3 ligase ligand, thalidomide (Cat. No. 0652). Potent, selective and cereblon-dependent degrader of CDK9 (EC50 = 4 nM). Displays >15-fold selectivity for CDK9 over other CDKs (EC50 values are 62, 171 and 398 nM for CDK2, CDK1 and CDK7, respectively). Induces complete degradation of CDK9 at 250 nM in MOLT4 cells. Inhibits proliferation of leukemia cell lines.
Sold under license from Dana-Farber Cancer Institute.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 869.02. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||1.15 mL||5.75 mL||11.51 mL|
|5 mM||0.23 mL||1.15 mL||2.3 mL|
|10 mM||0.12 mL||0.58 mL||1.15 mL|
|50 mM||0.02 mL||0.12 mL||0.23 mL|
References are publications that support the biological activity of the product.
Olson et al (2018) Pharmacological perturbation of CDK9 using selective CDK9 inhibition or degradation. Nat.Chem.Biol. 14 163 PMID: 29251720
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Keywords: THAL SNS 032, THAL SNS 032 supplier, THALSNS032, potent, selective, CDK9, degraders, degrades, PROTAC, proteolysis, targeting, chimera, Active, Degraders, Cyclin-dependent, Kinase, 6532, Tocris Bioscience
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
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Epigenetics in Cancer Poster
Adapted from the 2015 Cancer Product Guide Edition 3, this poster summarizes the main epigenetic targets in cancer. The dysregulation of epigenetic modifications has been shown to result in oncogenesis and cancer progression. Unlike genetic mutations, epigenetic alterations are considered to be reversible and thus make promising therapeutic targets.