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Merck

SML2601

Sigma-Aldrich

dTAG-13

≥98% (HPLC), powder, degradation tag  (dTAG) system

Sinónimos:

(2S)-(1R)-3-(3,4-Dimethoxyphenyl)-1-(2-(2-((6-((2-(2,6-dioxopiperidin-3-yl)-1,3-dioxoisoindolin-4-yl)oxy)hexyl)amino)-2-oxoethoxy)phenyl)propyl 1-((S)-2-(3,4,5-trimethoxyphenyl)butanoyl)piperidine-2-carboxylate, d-TAG-13

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About This Item

Fórmula empírica (notación de Hill):
C57H68N4O15
Número de CAS:
Peso molecular:
1049.17
UNSPSC Code:
12352200
NACRES:
NA.77

product name

dTAG-13, ≥98% (HPLC)

ligand

thalidomide

Quality Level

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear

storage temp.

−20°C

SMILES string

O=C(O[C@@H](C1=C(C=CC=C1)OCC(NCCCCCCOC2=C(C3=CC=C2)C(N(C3=O)C4CCC(NC4=O)=O)=O)=O)CCC5=CC=C(C(OC)=C5)OC)[C@@H]6CCCCN6C([C@H](C7=CC(OC)=C(C(OC)=C7)OC)CC)=O

Biochem/physiol Actions

dTAG-13 is a degradation tag (dTAG) system heterobifunctional degrader composed of an E3 ubiquitin ligase cereblon (CRBN)-binding thalidomide moiety and an FKBP12(F36V) mutant-specific ligand AP1867 void of affinity for endogenous (wild-type) FKBP12, allowing selective degradation of target proteins of interest when expressed as an FKBP12(F36V) in-frame fusion (by transgene expression or locus-specific knock-in) by bridging them with CRBN for ubiquitination. dTAG-13 is shown to potently degrade FKBP12F36V-MELK(sg3R) in MDA-MB-468 cells (100 nM for 4 hrs) as well as ENL-FKBP12F36V-HA, but not endogenous ENL, in MV4;1 cells (500 nM for 0.5-1 hrs).

Other Notes

Contains a mixture of diastereomers. This product has not been tested in cellular degradation assays.

Legal Information

Sold with permission under license from Dana Farber Cancer Institute.

Related product

Referencia del producto
Descripción
Precios

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

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Michael A Erb et al.
Nature, 543(7644), 270-274 (2017-02-28)
Recurrent chromosomal translocations producing a chimaeric MLL oncogene give rise to a highly aggressive acute leukaemia associated with poor clinical outcome. The preferential involvement of chromatin-associated factors as MLL fusion partners belies a dependency on transcription control. Despite recent progress
The dTAG system for immediate and target-specific protein degradation.
Nabet B, Roberts JM, Buckley DL, et al.
Nature Chemical Biology, 14(5), 431-441 (2018)
MELK is not necessary for the proliferation of basal-like breast cancer cells
Huang HT, Seo HS, Zhang T, et al.
eLife, 6, e26693-e26693 (2017)
Transcription control by the ENL YEATS domain in acute leukaemia
Erb MA, Scott TG, Li BE, et al.
Nature, 543(7644), 270-274 (2017)
Ricardo Linares-Saldana et al.
Nature genetics, 53(10), 1480-1492 (2021-10-07)
Higher-order chromatin structure regulates gene expression, and mutations in proteins mediating genome folding underlie developmental disorders known as cohesinopathies. However, the relationship between three-dimensional genome organization and embryonic development remains unclear. Here we define a role for bromodomain-containing protein 4

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